Character Development

Patient. SSG Marcus “Prophet” Washington, 29 — Civil Affairs NCO, third Africa deployment. Meticulous about antimalarial prophylaxis until his pills fell into a latrine pit three days ago during a MEDCAP in rural Somalia. Rather than report the loss and risk being pulled, he decided to “tough it out” for the remaining week.

Medic. SFC James “Doc” Okonkwo, 34 — SF Medical Sergeant of Nigerian heritage, fluent in Hausa, Yoruba, and French. He has treated dozens of malaria cases and knows P. falciparum does not negotiate.

Environment

Before. Remote village in Jubbaland, Somalia, 180 km from Mogadishu. A 6-man ODA conducts a week-long assessment with local clan militia. Austere conditions — sleeping in a compound shared with livestock. Rainy season has left standing water everywhere; mosquitoes are relentless despite treated uniforms and DEET. Nearest Role 2 is in Mogadishu, reachable only by helicopter or a road controlled by al-Shabaab.

During. Day 5. SSG Washington wakes at 0300 with violent chills despite 85°F ambient temp, teeth chattering. By morning: high fever, severe headache, vomiting — he blames “something I ate.” By 1400 he is barely responsive, speaking incoherently about his daughters. Okonkwo recognizes the pattern immediately. Next MEDEVAC window is 36 hours out and weather is deteriorating.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE SEVERE MALARIA: AMS, jaundice, renal impairment, hypotension = life-threatening emergency.
• IV ACCESS: two large-bore IVs — needs both fluids and antimalarial therapy.
• ANTIMALARIAL: IV artesunate 2.4 mg/kg (≥20 kg) at 0/12/24 h then daily — first-line (CDC 2024, WHO 2024).
• IF NO ARTESUNATE: IM artemether 3.2 mg/kg load then 1.6 mg/kg daily; quinine only as last resort.
• FLUIDS: cautious NS/LR — monitor closely for pulmonary edema.
• GLUCOSE: check q4h; D50 if <70 mg/dL (profound, recurrent hypoglycemia).
• FEVER CONTROL: acetaminophen, cooling — hyperthermia worsens cerebral malaria.
• SEIZURES: midazolam ready; do NOT give prophylactic anticonvulsants.
• URINE OUTPUT: target >0.5 mL/kg/hr; dark urine = hemolysis/blackwater fever.
• AVOID: steroids (harmful), aspirin (bleeding); EXCHANGE TRANSFUSION no longer recommended (CDC 2024).
• EVACUATE: URGENT — severe malaria needs ICU care; initiate 9-line immediately.

Clinical Pearls

• P. falciparum is the only species that routinely causes severe/cerebral malaria and can kill within hours.
• Jaundice + dark urine = hemolysis (blackwater fever) — massive RBC destruction.
• Hypoglycemia is common and recurrent — check glucose frequently.
• HRP2-based RDTs can be falsely negative in the Horn of Africa (pfhrp2/3 deletions) — treat on suspicion.
• IV artesunate is first-line (CDC 2024); exchange transfusion is no longer recommended.
• Watch for post-artesunate delayed hemolysis (PADH) 1–3 weeks out — brief the receiving team.

Character Development

Patient. CPT Alejandro “Raptor” Moreno, 32 — SF Detachment Commander, West Point grad, former Ranger. Received yellow fever vaccine 11 years ago; the booster requirement was waived for op-tempo. Leading his ODA through the jungle regions of the DRC tracking an ADF splinter group.

Medic. SSG Rafael “Santos” Delgado, 30 — senior medic, USUHS tropical-medicine training, with a standing interest in viral hemorrhagic fevers after a near-miss Ebola exposure. He has never seen yellow fever but has read every case report he can find.

Environment

Before. Dense rainforest, North Kivu Province, DRC. Two weeks in the jungle on recon/surveillance. Canopy too thick for helicopter extraction without clearing; 72 hours from the nearest road, 200 km from the nearest facility in Goma. Yellow fever is endemic; prime mosquito habitat.

During. Day 14: sudden high fever, severe headache, photophobia — “jungle crud.” Brief apparent recovery days 3–4. Day 17: severe epigastric pain, hematemesis, visible jaundice, spontaneous gum bleeding. Delgado realizes this is neither malaria nor typhoid.

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Vital Signs

Physical Examination

Critical Actions

• ISOLATION: standard + contact + droplet — VHF cannot be excluded clinically.
• IV ACCESS: minimal, careful — every needlestick is a potential exposure.
• NO SPECIFIC TREATMENT: supportive care only; no effective antiviral.
• FLUIDS: cautious crystalloid; PRBC/whole blood for hemorrhagic shock if available.
• AVOID ALL NSAIDs: aspirin/ibuprofen absolutely contraindicated — worsen bleeding.
• GLUCOSE: monitor frequently — liver failure causes hypoglycemia.
• GI BLEED: PPI (pantoprazole 40 mg IV) if available; TXA controversial.
• VITAMIN K: 10 mg IV/IM if available for coagulopathy.
• DOCUMENT EXPOSURE: all team members are now potential contacts.
• EVACUATE: URGENT to ICU + blood-bank capability; coordinate with AFRICOM medical.

Clinical Pearls

• Faget sign (relative bradycardia with fever) is a powerful early clue.
• Biphasic course: fever → brief remission → toxic phase if it progresses.
• Most infections are mild; a minority reach the toxic phase, and of those roughly half die.
• “Black vomit” (vomito negro) = upper GI bleeding — ominous.
• A single vaccine dose is now considered lifelong for most (ACIP/WHO 2015) — do not over-rely on it diagnostically.
• Isolate for the VHF differential until PCR confirms, even though YF is not efficiently person-to-person.

Character Development

Patient. PFC Devon “Rookie” Jackson, 20 — arrived at Camp Lemonnier three days ago, first deployment, from Seattle. Trying to prove himself: volunteering for every working party, drinking energy drinks instead of water, skipping meals. Djibouti today is 118°F, 85% humidity.

Medic. SGT Yusuf “Chief” Abdullah, 28 — Ranger Medic attached to CJTF-HOA, the battalion heat-illness SME after treating a near-fatal case in Chad. He watches new arrivals like a hawk during acclimatization.

Environment

Before. Camp Lemonnier, August. WBGT 95°F — black-flag; PT suspended. Operational need requires moving equipment with mandatory rest/hydration cycles. Jackson keeps volunteering for “one more load.”

During. Two hours in, Jackson stumbles and nearly drops a 50-lb crate. Speech slurs; he asks if they're “still in Washington,” then collapses. Skin is hot and surprisingly dry. He begins seizing. Rectal temperature reads 107.2°F.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• COOL FIRST, TRANSPORT SECOND: cooling takes priority over everything except airway/breathing.
• TARGET: core <102°F within ~30 min — every minute of delay raises mortality.
• COLD-WATER IMMERSION: most effective — immerse to the neck if possible (tarp + ice water / TACO).
• NO IMMERSION? Rotating ice-water towels + ice to neck/axillae/groin; misting + fanning.
• STOP COOLING at 102°F to prevent overshoot hypothermia.
• SEIZURES: midazolam 5 mg IV/IM — seizing generates more heat.
• IV ACCESS: two large-bore; NS bolus, but surface cooling beats cold IV fluids.
• AVOID antipyretics (acetaminophen/NSAIDs) — ineffective and hepatotoxic in heat stroke.
• AIRWAY: protect during seizures; prepare to intubate if prolonged AMS.
• MONITOR: continuous core temp, urine output (rhabdo), mental status.
• EVACUATE: URGENT after initial cooling — high risk of multi-organ failure.

Clinical Pearls

• Hot, dry skin is ominous — but in exertional cases many patients are still sweating; diagnose on core temp + CNS.
• Cool FIRST, transport SECOND — endorsed by NATA and NAEMSP.
• Cold-water immersion is the gold standard (~0.15–0.20°C/min); never halt effective cooling to move.
• Antipyretics are useless in heat stroke — different mechanism than infectious fever.
• Rhabdomyolysis is nearly universal — monitor CK, push fluids, watch for dark urine.
• Multi-organ failure can appear 24–72 h after successful cooling.
• Acclimatization takes 10–14 days; new arrivals are the highest-risk group.

Character Development

Patient. Three of a six-man ODA conducting a FID rotation near Agadez, Niger. The index case is SFC Tomas “Griddle” Reyes, 35, the team's cook-by-habit, who shared a goat stew with partner-force soldiers two days ago. Two others have looser symptoms; Reyes is the sickest, with high fever and bloody stool.

Medic. SSG Hana “Mags” Magnusson, 31 — 18D on her second FID rotation. She has seen enough ‘Sahel belly’ to know the difference between the inconvenient and the dangerous, and she is tracking the outbreak as a force-health problem, not just three sick guys.

Environment

Before. A partner-nation compound outside Agadez at the edge of the Sahara. Water comes from a borehole of uncertain quality; the team has been mixing local food with rations to build rapport. Temperatures hit 110°F by midday. The nearest reliable medical support is the embassy clinic in Niamey, a full day's drive over contested road.

During. Reyes deteriorates over 36 hours: frequent watery stools become bloody and mucoid, fever spikes to 103°F, and he has cramping lower-abdominal pain and tenesmus. The other two have high-volume watery diarrhea without blood and are managing on oral fluids. Reyes is now orthostatic and can't keep up with losses.

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Vital Signs

Physical Examination

Critical Actions

• TRIAGE BY PATTERN: separate secretory (watery) from invasive (febrile/bloody) — different management.
• REHYDRATE: ORS first-line for all; IV/IO isotonic crystalloid for the orthostatic/shocked index case.
• EMPIRIC ANTIBIOTIC (febrile/dysenteric): azithromycin 1000 mg single dose (or 500 mg daily x3).
• AVOID loperamide monotherapy in febrile/bloody diarrhea; avoid if STEC suspected (HUS risk).
• RIFAXIMIN only for non-invasive watery TD — not for this patient.
• ZINC + continued feeding speed mucosal recovery; do not starve the gut.
• WATER/FOOD DISCIPLINE: treat all water; hot, freshly cooked food only; hand hygiene; latrine control.
• FORCE HEALTH: cohort cases, reassess fitness, file the reportable-medical-event report.
• REASSESS at 24–48 h: no response → consider amebiasis/C. diff/resistance, complications, evacuate.

Clinical Pearls

• ETEC is the most common cause of traveler's diarrhea — watery, secretory, fluid-loss is the threat.
• Fever + blood + tenesmus = invasive bacterial dysentery (Shigella, Campylobacter, invasive E. coli) — these get antibiotics.
• Azithromycin 1 g single dose is first-line for febrile/dysenteric TD; fluoroquinolone resistance (esp. Campylobacter) is now the rule, not the exception.
• ORS beats IV for most cases — sodium-glucose co-transport works even in secretory diarrhea.
• Never give loperamide alone in febrile/bloody diarrhea; never with suspected STEC.
• A diarrheal outbreak is a force-health emergency — water, food, and hygiene discipline win it.

Character Development

Patient. SGT Eli “Paperboy” Tran, 26 — a junior 18-series soldier on a village engagement in the Ethiopian highlands near Bahir Dar. A loose village dog bit him on the left forearm, breaking skin and drawing blood, while he tried to shoo it from a food cache. The dog ran off and could not be located or observed.

Medic. MSG Grace “Vowel” Owusu, 38 — senior SF medical sergeant who has run more MEDCAPs than she can count and treats every unprovoked mammal bite in the Horn of Africa as rabies until proven otherwise. She knows the math: rabies, once symptomatic, is essentially 100% fatal, and that PEP is the only lever that matters.

Environment

Before. A highland village at 1,800 m near Lake Tana. Dog-mediated rabies is endemic across rural Ethiopia, and stray dogs are everywhere around food sources. The team carries a basic medical kit but no rabies biologics; rabies immunoglobulin and vaccine are theoretically available in Addis Ababa, a half-day movement away, or through partner-nation public health.

During. Owusu examines two deep punctures and a 3-cm laceration on the volar forearm, actively bleeding, with surrounding tooth marks — a clear transdermal bite. Tran is up to date on tetanus and has never had rabies vaccine. There is no way to capture or observe the dog. The clock on PEP has started.

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Vital Signs

Physical Examination

Critical Actions

• WASH IMMEDIATELY: soap + water (± povidone-iodine/virucidal) for ≥15 minutes — highest-yield field action.
• DO NOT primarily suture if avoidable; if closure needed, infiltrate RIG first, then loose approximation.
• CATEGORIZE: transdermal bite that bled = WHO Category III → wound care + vaccine + RIG.
• RIG: human 20 IU/kg (equine 40 IU/kg), ONCE, by day 7 of vaccine; infiltrate into/around the wound (WHO 2018).
• VACCINE: start immediately — ID 2-site days 0/3/7, or IM days 0/3/7/14–28; deltoid, never gluteus.
• TETANUS: confirm/update status.
• ANTIBIOTIC PROPHYLAXIS: amoxicillin-clavulanate for the bite wound (Pasteurella + oral flora).
• DO NOT delay vaccine waiting on RIG; obtain RIG in parallel.
• DOCUMENT + TELECONSULT: exposure details, biologic lots/sites, schedule; coordinate public health and the next doses.
• EVACUATE/REFER to a facility with biologics if not on hand — non-negotiable priority.

Clinical Pearls

• Rabies, once symptomatic, is essentially 100% fatal — PEP is the only lever; treat every endemic-area mammal bite seriously.
• Immediate 15-minute soap-and-water wash is the single highest-yield field intervention.
• Category III = wound care + vaccine + RIG. There is no ‘wait and see’ for an unobservable animal.
• Infiltrate RIG INTO the wound (WHO 2018) — not a distant IM site; give it once, by day 7.
• Modern WHO regimens are short (1-week ID, or IM days 0/3/7/14–28); vaccine goes in deltoid, never gluteus.
• Never delay the vaccine waiting on RIG — start the series and chase the RIG in parallel.

Character Development

Patient. Pvt. Deng Akol, 24 — a partner-force soldier in a South Sudanese unit the ODA is advising along the Nile basin near Yei. Over two months his squad-mates noticed him becoming slow, sleeping through formations, then confused and irritable. He recalls a painful fly bite weeks earlier that left a sore. He is now somnolent by day and restless at night.

Medic. SFC Marcus “Quiet” Bell, 33 — 18D running partner-nation sick call. He has read about sleeping sickness but never seen it; what stops him is the reversed sleep cycle and a rubbery posterior cervical lymph node in a man from a tsetse-belt village.

Environment

Before. Riverine gallery forest near Yei, South Sudan — classic Glossina (tsetse) habitat. T. b. gambiense is endemic in West/Central Africa and accounts for the great majority of HAT. The disease is slow: hemolymphatic symptoms first, then, over weeks to months, invasion of the CNS. No U.S. medical facility is nearby; this is partner-force care with reach-back to WHO/NGO HAT programs that hold the specialized drugs.

During. Bell finds intermittent low fever, headache, generalized rubbery lymphadenopathy with a prominent posterior cervical node (Winterbottom sign), and a faint annular rash. Neuro exam shows daytime somnolence, a fine tremor, and slowed cognition. The history of a painful bite with a local chancre weeks earlier and a reversed sleep-wake cycle points hard at second-stage gambiense HAT.

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Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE THE PATTERN: tsetse exposure + chancre + Winterbottom sign + reversed sleep cycle = suspect HAT.
• DETERMINE LIKELY SUBSPECIES by geography: West/Central = gambiense (slow); East/Southern = rhodesiense (acute, emergency).
• DO NOT field-treat: HAT drugs and staging (lumbar puncture) belong to specialized WHO/NGO/national programs.
• STABILIZE + SUPPORT: nutrition, hydration, seizure precautions if CNS-involved.
• BROADEN DDx in HIV-prevalent areas: TB/cryptococcal meningitis, toxoplasmosis, cerebral malaria — require parasite demonstration to confirm HAT.
• REFER via reach-back to a HAT treatment center — urgent for rhodesiense, deliberate for gambiense.
• KNOW THE MODERN OPTION: oral fexinidazole (10 days, WITH food) for gambiense (and now rhodesiense) in eligible patients; NECT for CSF ≥100/µL or severe disease.
• DOCUMENT exposure, exam, and timeline for the receiving program.

Clinical Pearls

• Gambiense HAT (W/C Africa) is slow over weeks-months; rhodesiense (E/S Africa) is an acute emergency — geography tells you which.
• Winterbottom sign (posterior cervical lymphadenopathy) + reversed sleep-wake cycle are the classic clues.
• Staging by lumbar puncture (CSF cells/trypanosomes) historically drove drug choice and prognosis.
• Fexinidazole — the first all-oral cure (10 days, WITH food) — is now first-line for gambiense and, since 2024, rhodesiense in eligible patients; NECT for CSF ≥100/µL or severe disease.
• Untreated HAT is essentially always fatal; recognition + referral is the SOF medic's decisive contribution.
• In HIV-endemic areas, keep TB/cryptococcal meningitis and cerebral malaria on the differential — confirm HAT by finding the parasite.

Character Development

Patient. A 4-vehicle convoy near Manda Bay, Kenya, struck by a buried IED followed by small-arms fire. Four casualties: (A) SSG Pike — traumatic above-knee amputation, massive hemorrhage; (B) SGT Lowe — penetrating chest wound, respiratory distress; (C) SPC Day — altered, unequal pupils after blast, no external hemorrhage; (D) SrA Cruz — fragmentation wounds to the arm, walking, screaming. One medic, hostile contact ongoing.

Medic. SFC Dana “Anchor” Whitfield, 36 — the lone 18D on the ground, who has to run TCCC and mass-casualty triage simultaneously while the team suppresses the ambush. Her advantage is doctrine: MARCH, the phases of care, and the discipline to treat the right wound first.

Environment

Before. Coastal road near Manda Bay, scene of real al-Shabaab attacks on this airfield. The convoy is partner-force plus a small U.S. element. Role 2 surgical is in Mombasa; the 9-line and a tactical-evacuation plan are pre-briefed but the LZ is not yet secure.

During. The blast and ambush happen at once. Whitfield must apply Care Under Fire principles — win the firefight first, stop only the killable bleeding — then transition to Tactical Field Care as the team gains fire superiority. She faces four casualties, finite tourniquets and blood, and an evolving tactical picture.

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Vital Signs

Physical Examination

Critical Actions

• CARE UNDER FIRE: win the firefight; the only medicine is a tourniquet on extremity hemorrhage (self-aid if able).
• TRANSITION to Tactical Field Care once fire superiority is gained; then run MARCH on each casualty.
• M — Pike: limb tourniquet high/tight until bleeding stops; second TQ side-by-side if needed; mark time.
• R — Lowe: vented chest seal; needle decompression for tension (5th ICS AAL or 2nd ICS MCL).
• TRIAGE: T1 Pike + Lowe (salvageable, treatable killers); T2/T3 Cruz; agonize honestly over Day (severe TBI, one medic).
• TXA 2 g IV/IO single dose within 3 h for shock/major hemorrhage.
• WHOLE BLOOD is the resuscitation fluid of choice (walking blood bank); titrate to radial pulse / mentation.
• PERMISSIVE HYPOTENSION: target SBP ~100 mmHg (current TCCC) — perfuse the brain without popping clot.
• SCREEN BLAST INJURY in everyone near the blast: TMs, blast lung, occult abdominal — including 'walking wounded'.
• PREVENT HYPOTHERMIA even in heat — break the lethal triad (dry, insulate, active warming, warm fluids).
• EVACUATE by tactical priority: T1 first; push the 9-line; secure the LZ; document on TCCC cards.

Clinical Pearls

• Care Under Fire: win the firefight; the only medicine is a tourniquet — don't become casualty #5.
• MARCH order is deliberate: massive hemorrhage and the chest kill faster than anything you'd do later.
• Hemorrhage control + early whole blood + TXA (2 g, <3 h) is the modern survival package.
• Permissive hypotension (SBP ~100, current TCCC) perfuses the brain without blowing fresh clot.
• Triage is dynamic and does the greatest good for the greatest number — the severe TBI with one medic is the hardest, most honest call.
• Screen every blast casualty for occult injury — blast lung and TM rupture hide behind a 'walking' exterior.
• Hypothermia kills in the desert too — the lethal triad (hypothermia/acidosis/coagulopathy) doesn't care about ambient temperature.

Character Development

Patient. SPC Aisha “SparkPlug” Nwosu, 23 — a signals soldier at Camp Lemonnier on her fourth day of a febrile illness. The fever, which had been brutal, just broke — and instead of feeling better she now has worsening abdominal pain, vomiting, and a nosebleed. She had dengue once before, two years ago in a previous posting.

Medic. SSG Owen “Tide” Brennan, 32 — Ranger Medic who has learned the hard lesson that dengue is most dangerous when the fever LEAVES, not when it spikes. The defervescence-plus-warning-signs combination on day 4–5 is exactly what makes the hair on his neck stand up.

Environment

Before. Camp Lemonnier, Djibouti — Aedes aegypti is present in urban Horn-of-Africa settings and dengue circulates. A Role 2 with lab (CBC, hematocrit) is on the FOB, which is a major advantage; serial labs are the backbone of dengue management.

During. Day 4: the fever defervesces — the start of the critical phase. Over the next hours Nwosu develops severe, persistent abdominal pain, repeated vomiting, mucosal bleeding (epistaxis and gum oozing), and restlessness. Labs show a rising hematocrit with a falling platelet count. She has multiple WHO warning signs and a prior dengue infection — a setup for severe disease.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE THE CRITICAL PHASE: danger peaks at DEFERVESCENCE (day ~4–7), not at peak fever.
• SCREEN WARNING SIGNS (WHO 2009): abdominal pain, persistent vomiting, fluid accumulation, mucosal bleeding, lethargy/restlessness, liver >2 cm, rising HCT + falling platelets.
• SERIAL HCT + PLATELETS are the backbone of management — follow the trend.
• FLUIDS: titrated isotonic crystalloid (start ~5–7 mL/kg/h with warning signs), step down as she stabilizes; bolus for shock.
• INTERPRET HCT: rising HCT + unstable = leak (fluid); falling HCT + unstable = bleeding (blood).
• RECOVERY PHASE: BACK OFF fluids — reabsorbing plasma causes pulmonary edema.
• DO NOT transfuse platelets prophylactically; reserve blood products for significant bleeding/severe dengue.
• AVOID NSAIDs/aspirin and IM injections; use acetaminophen; exclude co-existing malaria.
• MONITOR every 1–2 h in the critical phase; lower evac threshold if no serial-lab capability.

Clinical Pearls

• Dengue's lethal window is the CRITICAL phase at defervescence — the patient looks worse when the fever leaves.
• Know the WHO 2009 warning signs cold — they exist to catch plasma leak before shock.
• A second infection with a different serotype is MORE dangerous (antibody-dependent enhancement) — prior dengue is a risk factor, not immunity.
• Serial hematocrit + platelets guide everything: rising HCT = leak (fluid); falling HCT = bleed (blood).
• Fluid management is a tightrope — too little = shock, too much (especially in recovery) = pulmonary edema.
• Do NOT transfuse platelets for a low count alone; avoid NSAIDs/aspirin; use acetaminophen.

Character Development

Patient. Most of an 8-soldier dive/recon element that crossed and swam in the Lake Victoria basin during a combined training exercise six weeks ago. Several developed an itchy rash ('swimmer's itch') days afterward and shrugged it off. Now four have fever, cough, hives, and malaise; the index case, SSG Priya “Otter” Nair, 30, is the sickest with high fever and wheezing.

Medic. SFC Cole “Ledger” Hammond, 35 — 18D who connects three dots most providers miss: the freshwater swim, the swimmer's itch weeks ago, and now a cluster of febrile, eosinophilic, wheezy soldiers. That triad in returnees from an African lake is acute schistosomiasis until proven otherwise.

Environment

Before. A training exercise in the Lake Victoria region — one of the most schistosomiasis-endemic freshwater systems on earth. Cercariae released by snails penetrate intact skin during freshwater contact. The element swam without barrier protection. Symptoms are appearing now, weeks after exposure, back at a FOB with reach-back to tropical-medicine consultants.

During. Six weeks post-exposure, the cluster develops the Katayama syndrome: fever, dry cough, urticaria, myalgia, and fatigue. Nair has high fever, audible wheeze, and migratory urticaria. A CBC (available at the FOB) shows marked eosinophilia. Stool/urine ova are not yet detectable — and serology may still be negative — because the worms have not started laying eggs.

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Vital Signs

Physical Examination

Critical Actions

• TAKE THE EXPOSURE HISTORY: connect today's fever/eosinophilia to freshwater contact weeks ago (Katayama lag is 2–8 wk).
• RECOGNIZE THE TRIAD: freshwater swim + swimmer's itch + febrile/wheezy/eosinophilic cluster = acute schistosomiasis.
• DON'T trust early-negative tests: ova and serology are often negative acutely — diagnose clinically; eosinophilia is the early clue.
• ACUTE MANAGEMENT: corticosteroids (e.g., prednisolone ~0.5 mg/kg/day short course) for the hypersensitivity reaction.
• PRAZIQUANTEL TIMING: do NOT rely on an early dose — it misses immature worms and can worsen symptoms; give/repeat at ~6–12 weeks once worms mature.
• EXCLUDE co-existing malaria; consider other migrating helminths.
• SCREEN THE WHOLE ELEMENT (including asymptomatic) with documented delayed follow-up testing.
• COUNSEL on complications (neuroschistosomiasis, chronic organ disease) and completing the later praziquantel course.
• PREVENT: avoid freshwater contact in endemic areas — treat any unavoidable exposure as a medical event.

Clinical Pearls

• Katayama fever appears 2–8 weeks AFTER freshwater exposure — take the remote exposure history or you'll miss it.
• Early stool/urine ova and serology are often negative; eosinophilia + exposure + syndrome makes the clinical diagnosis.
• Praziquantel kills adult worms only — an early dose misses immature schistosomula and can worsen symptoms; give/repeat at ~6–12 weeks.
• Corticosteroids are the mainstay of ACUTE management (hypersensitivity reaction); steroids can lower praziquantel levels.
• It's usually a cluster — screen and document the whole element, including the asymptomatic.
• Untreated infection becomes chronic: hepatosplenic/urogenital disease and rare neuroschistosomiasis — full treatment prevents lifelong morbidity.

Character Development

Patient. A roughly 2-year-old boy, 'Tesfaye,' brought by his mother to a MEDCAP in a drought-affected village in the Ethiopian lowlands. He is severely wasted ('skin and bones'), lethargic, with sunken eyes and a recent history of watery diarrhea. The mother says he stopped eating days ago. He has no edema but is profoundly thin with visible ribs.

Medic. SFC Maria “Bridge” Castellano, 37 — 18D leading the MEDCAP's pediatric station. She has the hardest discipline of all to hold here: the instinct to aggressively resuscitate and feed a starving, dehydrated child is exactly the instinct that can kill him. Severe malnutrition rewrites the rules of fluids and feeding.

Environment

Before. A medical civic-action program in a drought- and conflict-affected area where severe acute malnutrition (SAM) is endemic. The MEDCAP has basic supplies, ORS, some IV access capability, and — critically — a relationship with a local stabilization center / therapeutic feeding program. The mission is humanitarian assistance and partner capacity-building, not definitive pediatric critical care.

During. Castellano assesses a child with marasmic SAM and 'some dehydration' from diarrhea: lethargic, sunken eyes, slow skin pinch, but not in frank shock. He is hypothermic to touch and his blood sugar is likely low. The temptation — a big IV bolus and a hearty meal — is precisely what causes fatal fluid overload and refeeding syndrome in these children.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• DO NOT bolus IV fluids in a non-shocked SAM child — fluid overload/heart failure is a leading iatrogenic killer.
• REHYDRATE SLOWLY: ReSoMal (or diluted low-osmolarity ORS) orally/NG, ~5–10 mL/kg/h up to 12 h; reassess for overload.
• DO NOT use full-strength standard ORS — wrong sodium/potassium for SAM.
• TREAT HYPOGLYCEMIA: oral sugar/feed if alert, IV dextrose + immediate feed if unconscious; then feed q2–3 h day & night.
• TREAT HYPOTHERMIA: warm (kangaroo care, dry clothes, covered head), feed, recheck glucose.
• EMPIRIC ANTIBIOTICS: SAM masks infection — treat presumptively; don't wait for fever.
• FEED LOW & SLOW: stabilization with F-75 first (frequent small feeds) to avoid refeeding syndrome; F-100/RUTF only in rehabilitation phase.
• IV FLUIDS ONLY FOR TRUE SHOCK — cautiously, and stop once perfusion improves.
• HAND OFF to a therapeutic feeding program / stabilization center for the full WHO recovery pathway.
• AVOID creating dependency — build partner-nation capacity; don't attempt care you can't sustain.

Clinical Pearls

• In SAM, the rules flip: rehydrate SLOWLY (ReSoMal, oral/NG, ~5–10 mL/kg/h) — IV boluses cause fatal fluid overload.
• Never use full-strength standard ORS in SAM — too much sodium, too little potassium.
• Refeeding syndrome kills: start low and slow (F-75 stabilization first), then F-100/RUTF for rehabilitation.
• Hypoglycemia + hypothermia are linked markers of high mortality — treat both, feed frequently, and warm the child.
• SAM masks infection — give empiric antibiotics; hypothermia is more ominous than fever here.
• The decisive SOF-medicine move is restraint plus a warm handoff to a therapeutic feeding program — not a one-day rescue.

Character Development

Patient. SSG Daniel “Ledger” Park, 33 — a logistics NCO on a long FID rotation in northern Nigeria who has been eating off the local economy. He presents on day 8 of a stepwise rising fever with headache, abdominal pain, and constipation (not diarrhea), and looks toxic.

Medic. SFC Renata “Clock” Vasquez, 36 — 18D who knows that the classic 'malaria rule-out' fever in West Africa is often enteric fever, and that the drug that would have worked ten years ago may now fail.

Environment

Before. A partner-nation garrison outside Kano, Nigeria. Food and water hygiene is inconsistent; Park has been the guy who eats whatever the partner force offers to build rapport. Lab is limited to a malaria RDT and a basic CBC; blood culture must be sent out.

During. Vasquez finds a sustained fever that climbs each evening, relative bradycardia, a tender abdomen, hepatosplenomegaly, and a few faint blanching 'rose spots' on the trunk. The malaria RDT is negative. Park is becoming confused ('typhoid state').

OPQRST

Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE THE PATTERN: stepwise fever + Faget sign + rose spots + hepatosplenomegaly + food exposure = enteric fever.
• DON'T anchor on a negative malaria RDT — co-infection is common; keep treating/ruling out malaria.
• BLOOD CULTURES before antibiotics if any reach-back lab exists.
• EMPIRIC ANTIBIOTIC (assume resistance): azithromycin (1 g load then 500 mg/d x7), OR carbapenem for severe/XDR; ceftriaxone 2 g/d only where ceftriaxone resistance not established.
• DEXAMETHASONE for severe disease with shock/altered mentation.
• ANTICIPATE perforation (sudden rigidity/peritonitis) and GI hemorrhage in week 2-3 — surgical evacuation.
• FLUIDS/electrolytes; antipyretics; monitor mental status and abdomen serially.
• FORCE HEALTH: water/food/hygiene/latrine discipline; consider TCV; reportable medical event.
• EVACUATE for surgical abdomen, hemorrhage, or failure to improve.

Clinical Pearls

• Enteric fever is a leading cause of 'malaria-negative' fever in West Africa — stepwise fever, Faget sign, rose spots.
• Resistance now drives drug choice: XDR/H58 S. Typhi resists fluoroquinolones and (in XDR) ceftriaxone — azithromycin or carbapenem are the reliable options.
• Malaria and typhoid coexist — a negative malaria RDT does not let you stop thinking about malaria.
• Week 2-3 brings perforation and GI hemorrhage — sudden rigidity = surgical evacuation.
• Recovered patients can become chronic gallbladder carriers — a force-health issue for food handlers.
• Typhoid conjugate vaccine + water/food/hygiene discipline are the prevention backbone.

Character Development

Patient. A 40-year-old man in a flood-displaced community where a SOF element is running a humanitarian-assistance mission near the Niger Delta. He arrives carried by relatives after hours of explosive watery diarrhea, now barely conscious, with sunken eyes and no palpable radial pulse. Several other villagers are sick.

Medic. SFC Tomas “Wellspring” Iverson, 35 — 18D who recognizes that cholera doesn't kill by toxin, it kills by the speed of water loss, and that the entire game is replacing volume as fast as it pours out.

Environment

Before. A flooded delta settlement during a cholera outbreak — contaminated water, crowding, and a collapsed sanitation system. The element has Ringer's lactate, ORS sachets, and is coordinating with an NGO cholera treatment center, but the nearest is hours away.

During. Iverson finds 'rice-water' stool, profound dehydration, tachycardia, an unrecordable blood pressure, and cool mottled skin — hypovolemic shock from pure fluid loss. The man can't drink. The clock is measured in minutes.

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Vital Signs

Physical Examination

Critical Actions

• RAPID IV REHYDRATION: Ringer's lactate ~100 mL/kg over ~3 h for severe dehydration; push ~30 mL/kg in the first 30 min until radial pulse returns.
• MULTIPLE LINES / IO as needed — do not under-resuscitate; replace ongoing stool losses volume-for-volume.
• START ORS by mouth as soon as the patient can drink (provides potassium + glucose RL lacks).
• ANTIBIOTIC (severe, after vomiting stops): doxycycline 300 mg single dose (or azithromycin 1 g; cipro only if resistance).
• MONITOR/REPLACE potassium; watch for hypoglycemia (glucose, esp. children) and acidosis.
• WATCH for fluid overload once perfusion returns — reassess frequently, titrate.
• ZINC for children <5.
• OUTBREAK CONTROL: feed into cholera treatment center; safe water, sanitation, hand hygiene, safe burials, OCV; protect the team.

Clinical Pearls

• Cholera kills by speed of fluid loss — rapid, large-volume Ringer's lactate is the entire game.
• Severe dehydration ≈ 10% body weight: ~100 mL/kg over 3 h, with the first push in the first 30 min.
• RL is potassium-poor — start ORS early for potassium and glucose; anticipate hypokalemia and hypoglycemia.
• Antibiotics (single-dose doxycycline; azithromycin alt) are adjunctive — they never replace fluids.
• Untreated CFR >50%; with prompt rehydration <1% — the basics, done fast, win.
• It's an outbreak: water, sanitation, hygiene, safe burials, and OCV protect the population and the team.

Character Development

Patient. A 19-year-old partner-force recruit in a crowded barracks in northern Burkina Faso during the dry season. He went from headache and fever to neck stiffness, photophobia, and a spreading petechial-then-purpuric rash within hours. Two other recruits have fevers.

Medic. SFC Aimee “Beacon” Okafor, 34 — 18D advising the partner force, who knows the meningitis belt turns deadly in the Harmattan dust season and that minutes of delay in giving ceftriaxone cost lives and brains.

Environment

Before. A partner-nation training barracks in the Sahel during Harmattan (dry, dusty, Dec–June) — the meningitis-belt epidemic season, with crowding accelerating transmission. Ceftriaxone is on hand; the nearest hospital is hours over rough road.

During. Okafor finds a stuporous recruit with nuchal rigidity, a positive Kernig sign, photophobia, and a non-blanching purpuric rash that is visibly spreading — meningococcemia with meningitis and early septic shock. This is a 'treat in the next few minutes' emergency.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• TREAT ON SUSPICION: meningismus + fever in the belt during dry season = meningococcal meningitis until proven otherwise.
• CEFTRIAXONE NOW: 2 g IV/IM (weight-based peds), minimum 5 days (WHO) — before LP, imaging, or transport.
• DEXAMETHASONE early with/before first antibiotic (don't delay antibiotics for it).
• TEST/TREAT MALARIA in parallel — co-endemic, overlapping presentation.
• SEPTIC SHOCK: IV/IO fluids titrated to perfusion; anticipate DIC and adrenal insufficiency (purpura fulminans).
• DROPLET PRECAUTIONS for first 24 h of treatment.
• CONTACT PROPHYLAXIS: single-dose ciprofloxacin / ceftriaxone / rifampin for close contacts.
• NOTIFY host-nation public health + higher medical; cohort cases; consider Men5CV campaign.
• EVACUATE emergently — fulminant disease.

Clinical Pearls

• African meningitis belt + Harmattan dry season + crowding = peak meningococcal epidemic risk.
• Antibiotics BEFORE LP/imaging/transport — ceftriaxone 2 g, minimum 5 days (WHO no longer endorses single-dose).
• Spreading non-blanching purpura + shock = meningococcemia/purpura fulminans — treat septic shock + DIC, evacuate.
• Co-endemic malaria can mimic/coexist — test and treat in parallel.
• Close contacts get single-dose chemoprophylaxis (cipro/ceftriaxone/rifampin); notify public health.
• Men5CV (NmCV-5), WHO-prequalified 2023, is the durable belt countermeasure.

Character Development

Patient. SSG ChiomaEze 'Marathon' Brown, 31 — a SOF soldier on a sustained mission in rural Sierra Leone who slept in rodent-accessible structures. She presents with ~10 days of insidious fever, severe sore throat, retrosternal pain, and now bleeding gums and facial/neck swelling.

Medic. SFC Peter “Quarantine” Adeyemi, 37 — 18D with tropical-medicine training who knows Lassa is the West African VHF that hides as 'just a bad flu' for a week before turning, and that the standard drug for it rests on shaky evidence.

Environment

Before. Rural Sierra Leone in Lassa-endemic country — Mastomys rodent contact via food/dust contamination is the route, and person-to-person spread via body fluids is a real risk in care. The element has reach-back to AFRICOM medical and a path to an isolation-capable facility.

During. Adeyemi sees the ominous progression: pharyngitis without much cough, retrosternal pain, proteinuria, mucosal bleeding, and the classic facial/neck edema of severe Lassa. Hearing loss is developing. He must protect the team while pushing evacuation.

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Vital Signs

Physical Examination

Critical Actions

• ISOLATE: standard + contact + droplet precautions; PPE; minimize sharps/aerosols — VHF cannot be excluded and Lassa spreads via body fluids.
• SUPPORTIVE CARE IS THE MAINSTAY: fluids/electrolytes, perfusion, correct coagulopathy, transfuse for bleeding, renal support.
• RIBAVIRIN: consider case-by-case with specialist/teleconsult input — evidence is weak/contested; do NOT treat as a settled reflex.
• TEST/TREAT malaria and typhoid in parallel (co-endemic, treatable).
• DOCUMENT all contacts; consider PEP for high-risk contacts per protocol.
• NOTIFY higher + receiving facility early; PCR confirmation via reference lab.
• SPECIAL CAUTION in pregnancy — very high maternal/fetal mortality.
• RODENT CONTROL / food protection prevents primary exposure.
• EVACUATE to isolation-capable facility — containment and evacuation run in parallel.

Clinical Pearls

• Lassa is insidious — a week-plus 'bad flu' before it turns; pharyngitis, retrosternal pain, facial/neck edema, and hearing loss are clues.
• You can't distinguish VHFs clinically — isolate on suspicion + exposure; PCR confirms.
• Ribavirin evidence is weak and possibly harmful in mild disease — teach the controversy; supportive care is the mainstay.
• Lassa spreads person-to-person via body fluids — contact/droplet PPE protects caregivers.
• Sensorineural hearing loss is a hallmark, often permanent sequela.
• Pregnancy (esp. 3rd trimester) carries very high mortality — flag it.

Character Development

Patient. A partner-nation soldier in the Kagera region near the Rwanda–Tanzania border who explored a bat-infested mine three weeks ago. He presents with abrupt high fever, severe headache and malaise, then watery diarrhea, vomiting, and — by day 6 — bleeding from multiple sites. A barracks-mate who cared for him is now also febrile.

Medic. SFC Lena “Containment” Hartmann, 36 — 18D advising in a region with recent Marburg outbreaks, acutely aware that this filovirus has no approved treatment, spreads readily to caregivers, and killed mostly healthcare workers in the 2024 Rwanda outbreak.

Environment

Before. Kagera region — site of Tanzania's 2023 and 2025 Marburg outbreaks and adjacent to Rwanda's 2024 outbreak (66 cases, 23% CFR, 77% in healthcare workers; index linked to Egyptian fruit-bat exposure at a mine). Egyptian fruit bats are the reservoir; human-to-human spread is via body fluids. Reach-back exists to a VHF treatment center.

During. Hartmann recognizes the filovirus pattern: abrupt onset, the incubation matching a bat-cave/mine exposure ~3 weeks prior, severe GI losses, and now multifocal bleeding around day 6–9. A caregiver contact is symptomatic — the nosocomial signature of Marburg. There is no specific drug; isolation and supportive care are everything.

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Vital Signs

Physical Examination

Critical Actions

• ISOLATE IMMEDIATELY on suspicion: full VHF PPE, strict isolation/cohorting, minimize sharps/aerosols.
• NO APPROVED DRUG: supportive care is the therapy — aggressive fluids/electrolytes for massive GI losses, perfusion support.
• TRANSFUSE / manage coagulopathy for hemorrhage; glucose; antiemetics/antidiarrheals for volume control.
• TEST/TREAT malaria + bacterial sepsis empirically in parallel (co-endemic, treatable).
• RT-PCR via reference lab to confirm and DISTINGUISH from Ebola (which has approved mAbs).
• PROTECT CAREGIVERS — most 2024 Rwanda cases were healthcare workers; safe body-fluid/linen handling; safe dignified burials.
• NOTIFY host-nation public health + AFRICOM/WHO/Africa CDC; contact tracing + 21-day monitoring.
• EVACUATE/REFER to a VHF treatment center; containment and evacuation in parallel.

Clinical Pearls

• Marburg has NO approved drug or vaccine — early aggressive supportive care is the therapy (Rwanda 2024 CFR 23% vs historical ~50%).
• Marburg and Ebola are clinically identical — PCR differentiates, and only Ebola has approved mAbs (Inmazeb/Ebanga).
• Reservoir is the Egyptian fruit bat (caves/mines); human-to-human spread is via body fluids.
• Caregivers are the highest-risk casualties — most 2024 Rwanda cases were healthcare workers; PPE and safe burials are decisive.
• Massive GI fluid loss kills — resuscitate volume aggressively while managing hemorrhage.
• Recognize, isolate, support, notify, refer — the SOF medic breaks the chain, the outbreak system cures.

Character Development

Patient. WO 'Steady' Mutombo, 42 — a long-serving partner-force officer in eastern DRC whom the ODA has worked alongside for months. He has months of cough (now productive of blood-streaked sputum), drenching night sweats, fever, and 20 lbs of weight loss. He was 'treated for TB' once before but didn't finish the pills.

Medic. SFC Owen “Marathon” Reilly, 35 — 18D who recognizes a chronic-cough partner officer as a TB problem with two implications: a transmission risk to the whole team, and the very real possibility of drug-resistant disease given the prior incomplete treatment.

Environment

Before. Eastern DRC, a high-TB-burden setting with significant HIV co-infection and circulating drug-resistant strains. The team has shared enclosed spaces and vehicles with Mutombo for months. GeneXpert and a TB program are reachable through partner-nation/NGO channels.

During. Reilly puts together the chronic cough, hemoptysis, night sweats, weight loss, and the history of interrupted prior treatment — a textbook setup for drug-resistant TB — and immediately thinks about both diagnosis (GeneXpert for TB + rifampin resistance) and protecting the team that's been breathing the same air for months.

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Vital Signs

Physical Examination

Critical Actions

• SUSPECT DRUG-RESISTANT TB: chronic cough/hemoptysis/night sweats/weight loss + prior incomplete treatment.
• DIAGNOSE via referral: GeneXpert MTB/RIF (TB + rifampin resistance in ~2 h), then culture/DST.
• DON'T field-treat: route to a partner-nation/NGO TB program holding the regimens.
• KNOW THE REGIMEN: 6-month all-oral BPaLM (bedaquiline, pretomanid, linezolid, moxifloxacin) for MDR/RR/pre-XDR TB (WHO 2022/2024).
• INFECTION CONTROL: mask the patient, ventilate spaces, respiratory protection (N95) for the team, separate quarters.
• FORCE HEALTH: report exposure; screen the team (symptom screen + testing + imaging) per protocol.
• EVALUATE HIV status (high regional prevalence; strongest risk factor for active TB) and co-manage.
• SUPPORT ADHERENCE — incomplete treatment breeds resistance; the all-oral 6-month course aids completion.

Clinical Pearls

• Prior incomplete TB treatment is the classic driver of drug resistance — a huge red flag in a chronic-cough patient.
• GeneXpert MTB/RIF diagnoses TB and rifampin resistance in ~2 hours — the gateway to MDR-TB care.
• BPaLM (6-month, all-oral: bedaquiline, pretomanid, linezolid, moxifloxacin) revolutionized MDR/RR-TB (TB-PRACTECAL ~89% vs ~52% success).
• TB is airborne — a coughing, untreated partner shared months of enclosed air with the team; protect and screen the force.
• HIV is the strongest risk factor for active TB — co-evaluate in this region.
• The SOF role is recognize, protect, refer, and support adherence — not run the regimen.

Character Development

Patient. SGT 'Suture' Bia, 27 — a junior medic on the ODA who sustains a deep hollow-bore needlestick to the thumb while starting an IV on a bleeding, hemodynamically unstable local national of unknown HIV status during a MEDCAP in eastern DRC.

Medic. MSG Dolores “Clock” Park, 39 — senior 18D who treats an occupational bloodborne exposure as a stopwatch event: the higher-risk the exposure and the faster PEP starts, the better, and in a high-prevalence region you act first and risk-stratify in parallel.

Environment

Before. A MEDCAP in a high-HIV-prevalence region with limited rapid testing. The source patient is unstable and can't reliably consent to or complete testing in the moment. The team carries a starter course of antiretrovirals; the embassy clinic has full PEP and baseline labs.

During. Park assesses a deep, blood-visible, hollow-bore needlestick (high-risk features), washes the wound, and recognizes the decision is time-sensitive: PEP works best started within hours and should not wait on source-patient testing that may never come.

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Vital Signs

Physical Examination

Critical Actions

• FIRST AID: wash with soap and water; let it bleed gently; no squeezing/caustics/bleach.
• START HIV PEP ASAP (within hours; not >72 h) — don't wait on source testing in a high-risk exposure.
• REGIMEN: 28 days, 3-drug INSTI-based — bictegravir/FTC/TAF (Biktarvy) OR dolutegravir + TAF/TDF + FTC/3TC (2025 USPHS).
• BASELINE LABS (provider): HIV Ag/Ab ± RNA, HBV status, HCV Ab, renal/hepatic, pregnancy; follow-up HIV testing ~6 wk & 3–4 mo.
• HEPATITIS B: check immunity; HBIG ± vaccine if non-immune and source positive/unknown.
• HEPATITIS C: no PEP — baseline + follow-up testing; treat if seroconversion (curable with DAAs).
• SOURCE: attempt consented rapid testing in parallel; a reliably negative source can justify stopping PEP.
• DOCUMENT exposure; counsel on adherence, side effects, and interim precautions; arrange continuation.

Clinical Pearls

• HIV PEP is a stopwatch: start within hours, not beyond 72 h — don't wait on source testing for a high-risk exposure.
• Regimen is 28 days, 3-drug INSTI-based (Biktarvy, or dolutegravir-based) per 2025 USPHS guidance.
• Wash with soap and water; let it bleed — don't squeeze or use caustics.
• It's a three-pathogen problem: HBV (check immunity, HBIG if needed) and HCV (no PEP; test and treat) too.
• A reliably negative source can justify stopping PEP — but the provider's first dose shouldn't wait for it.
• The SOF medic runs the highest-risk procedures with the least safety net — self-protection is a core skill.

Character Development

Patient. SSG 'Boots' Calloway, 30 — bitten on the lower leg by a puff adder he stepped near while moving through brush at dusk in rural Kenya. Within an hour the limb is grossly swollen, dark, and exquisitely painful, with blistering and oozing from the fang marks.

Medic. SFC Ravi “Anchor” Nair, 36 — 18D who knows African snakebite splits into two very different problems — cytotoxic (tissue-destroying) versus neurotoxic (paralyzing) — and that the right first aid for one is the wrong first aid for the other.

Environment

Before. Rural Kenyan bush at dusk — prime puff-adder territory; the puff adder causes a large share of serious African bites because it's common, well-camouflaged, and doesn't flee. Antivenom (SAIMR polyvalent) is at a regional hospital hours away; the team kit has none.

During. Nair sees rapidly advancing local tissue destruction — massive swelling, blistering, ecchymosis, and necrosis — plus oozing that signals venom-induced coagulopathy. He must resist the instinct to apply a tight tourniquet or pressure wrap, which would concentrate necrotic venom, and instead manage limb, coagulopathy, and rapid evacuation to antivenom.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• IDENTIFY THE SYNDROME: cytotoxic (viper — local necrosis/coagulopathy) vs neurotoxic (elapid — paralysis). This bite is cytotoxic.
• NO TOURNIQUET / NO PRESSURE-IMMOBILIZATION for cytotoxic bites — it concentrates necrotic venom.
• DO: calm/still patient, remove rings/constrictors, splint + elevate to heart level, mark swelling edge with time, treat pain.
• DON'T: cut, suck, ice, shock, or use traditional remedies.
• EVACUATE URGENTLY to antivenom — the only definitive treatment (regional polyvalent, e.g., SAIMR).
• ANTIVENOM INDICATIONS: coagulopathy/systemic bleeding, shock, advancing local necrosis, AKI — patient qualifies.
• PREP FOR ANAPHYLAXIS before infusing antivenom: epinephrine, IV fluids, airway ready.
• MONITOR compartment syndrome + coagulopathy; defer fasciotomy until coagulopathy corrected; correct bleeding with antivenom ± products.
• TETANUS update; watch for secondary infection.

Clinical Pearls

• African snakebite splits into cytotoxic (vipers: necrosis + coagulopathy) and neurotoxic (elapids: paralysis) — first aid differs.
• Pressure immobilization is for neurotoxic elapid bites WITHOUT necrosis — it's CONTRAINDICATED for cytotoxic viper bites (concentrates venom).
• No tourniquet, no cutting/sucking/ice/traditional remedies — remove constrictors, splint, mark swelling, evacuate.
• Antivenom is the only definitive treatment — give for coagulopathy, bleeding, shock, advancing necrosis; prep for anaphylaxis.
• Watch compartment syndrome and coagulopathy; correct bleeding with antivenom before any fasciotomy.
• Snakebite is a WHO-priority NTD (~81,000–138,000 deaths/yr) — a real dismounted-bush casualty mechanism.

Character Development

Patient. A partner-force soldier in the Ethiopia–Sudan borderlands with weeks-to-months of irregular fever, dramatic weight loss, a grossly enlarged spleen, darkening skin, and progressive pancytopenia (pallor, bruising, recurrent infections).

Medic. SFC Dana “Ledger” Cole, 35 — 18D who recognizes that a chronically wasting, massively splenomegalic, pancytopenic soldier from the East African kala-azar belt has visceral leishmaniasis until proven otherwise — a disease that is nearly always fatal untreated.

Environment

Before. The East African VL focus (Ethiopia, Sudan, South Sudan, Kenya) — one of the world's highest-burden kala-azar regions — where the sandfly transmits Leishmania donovani. HIV co-infection is common and worsens prognosis. Specialized treatment lives in NGO/national VL programs reachable through reach-back.

During. Cole finds the classic kala-azar tetrad: chronic irregular fever, massive splenomegaly, profound weight loss/wasting, and pancytopenia, with the hyperpigmentation that gives the disease its name ('black fever'). This is a refer-to-program diagnosis, not a field-treat one.

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Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE THE TETRAD in the East African focus: chronic irregular fever + massive splenomegaly + wasting + pancytopenia (± hyperpigmentation) = VL.
• DON'T field-treat: refer to an NGO/national VL program for diagnosis (rK39 serology, aspirate/PCR) and therapy.
• KNOW THERAPY: East African antimonial-based (± paromomycin), with liposomal amphotericin B and miltefosine increasingly used.
• TEST HIV — co-infection worsens prognosis and mandates COMBINATION therapy (liposomal ampho B + miltefosine) + ART + secondary prophylaxis.
• SUPPORTIVE CARE: nutrition, transfusion for severe anemia, aggressive treatment of intercurrent infections (neutropenia), bleeding precautions.
• PROTECT THE SPLEEN — rupture risk; avoid abdominal trauma.
• CO-EVALUATE for TB (co-endemic, mimics).
• TEAM PREVENTION: sandfly bite avoidance (permethrin, DEET, treated fine-mesh nets); no vaccine.

Clinical Pearls

• Kala-azar tetrad: chronic irregular fever + massive splenomegaly + wasting + pancytopenia (± 'black fever' hyperpigmentation).
• East Africa (Ethiopia/Sudan/South Sudan/Kenya) is a major L. donovani focus — fatal untreated.
• Diagnosis: rK39 serology + aspirate/PCR; treatment (antimonials ± paromomycin, liposomal ampho B, miltefosine) belongs to specialized programs.
• HIV co-infection worsens outcomes and mandates combination therapy + ART — always test.
• Death in VL often comes from intercurrent infection and bleeding — supportive care matters while awaiting cure.
• Sandflies bite at dusk/night and evade standard measures — permethrin/DEET/treated nets protect the team.

Character Development

Patient. A partner-force soldier in the Central African rainforest (Cameroon/Congo basin) being screened during a mass deworming/onchocerciasis effort. He's mostly asymptomatic but reports a worm once crawling across his eye and transient migratory limb swellings — and the team is about to hand out ivermectin to everyone.

Medic. SFC Ana “Firebreak” Mendez, 37 — 18D supporting a civil-affairs health effort who knows the single most dangerous thing she could do in this forest is give ivermectin reflexively to someone heavily infected with Loa loa.

Environment

Before. Central African rainforest where Loa loa (the African eyeworm, spread by Chrysops deerflies) is co-endemic with onchocerciasis. Ivermectin is the workhorse drug for oncho/filariasis mass drug administration — but in people with very high Loa microfilarial loads it can trigger fatal encephalopathy. Microscopy (day-blood mf counts) and a 'test-and-not-treat' strategy are the safeguards.

During. Mendez pauses the reflex. The eyeworm history and Calabar swellings flag possible heavy Loa infection, and giving ivermectin without knowing the microfilarial load could precipitate encephalopathy. The scenario's crisis is iatrogenic — the danger is the well-intentioned treatment itself.

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Vital Signs

Physical Examination

Critical Actions

• STOP the reflexive ivermectin in Loa-endemic forest zones — the routine drug is the hazard here.
• FLAG high-Loa risk: eyeworm history, Calabar swellings, high eosinophilia.
• TEST-AND-NOT-TREAT: measure daytime-blood Loa microfilarial load; withhold ivermectin if load is high (>~30,000 mf/mL).
• REFER high-load loiasis to specialists — albendazole (slow, safer mf reduction), apheresis, or cautious DEC under expert oversight.
• DON'T give DEC empirically — it can cause severe reactions/encephalopathy in high-load patients.
• IF POST-TREATMENT ENCEPHALOPATHY: airway, seizure control, hemodynamic support, urgent evacuation; exclude/treat malaria & meningitis in parallel.
• DOCUMENT and coordinate with the host-nation/NGO MDA program.
• PREVENTION emphasis — there is no antidote once encephalopathy is established.

Clinical Pearls

• Ivermectin can cause FATAL encephalopathy in patients with very high Loa loa loads (>~30,000 mf/mL) — onset ~1–2 days post-dose.
• In Loa-endemic forest zones, use 'test-and-not-treat': measure daytime Loa microfilarial load before giving ivermectin.
• Eyeworm history + Calabar (migratory) swellings + eosinophilia = possible heavy loiasis — a red flag against reflexive treatment.
• High-load loiasis is a specialist problem (albendazole/apheresis; DEC only with caution) — don't improvise.
• Post-ivermectin Loa encephalopathy has no antidote — prevention is everything; manage established cases with neurocritical support + evacuation.
• 'Do no harm' is an active decision — the trained medic stops a routine protocol when local epidemiology makes it dangerous.

Character Development

Patient. SSG 'Climber' Tate, 31 — part of an element that ascended rapidly to ~4,500 m on an operation in the Ethiopian highlands. He developed headache, nausea, and insomnia (AMS), then over 12 hours became ataxic and confused (HACE); a teammate is now breathless at rest with a cough productive of frothy sputum (HAPE).

Medic. SFC Lena “Thin-Air” Brooks, 35 — 18D who knows the cardinal rules of altitude: ataxia and altered mentation mean the brain is swelling, breathlessness at rest with frothy sputum means the lungs are flooding, and for both the definitive treatment is the same word — DESCEND.

Environment

Before. A rapid ascent to high altitude in the Ethiopian highlands (operationally, also relevant to Kilimanjaro and the Atlas) without time to acclimatize. The element has acetazolamide, dexamethasone, nifedipine, and supplemental oxygen, but is high on a mountain with descent the only definitive option.

During. Brooks faces two severe altitude emergencies at once: HACE (ataxia, confusion progressing toward coma) in Tate and HAPE (dyspnea at rest, frothy/pink sputum, crackles, hypoxia) in his teammate. Both are killers, both share the same definitive fix, and the mountain is fighting her.

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Vital Signs

Physical Examination

Critical Actions

• DESCEND — the definitive treatment for both HACE and HAPE; do it as soon as safely possible, don't wait on drugs.
• RECOGNIZE EMERGENCIES: ataxia/confusion = HACE; rest dyspnea + frothy sputum + hypoxia = HAPE.
• OXYGEN to both (prioritize the hypoxic HAPE casualty); portable hyperbaric (Gamow) bag if descent blocked.
• HACE: dexamethasone (8 mg load, then 4 mg q6h) ± acetazolamide.
• HAPE: nifedipine ER (± sildenafil/tadalafil) + oxygen; minimize exertion.
• KEEP WARM; minimize exertion (worsens HAPE); continuous reassessment for progression to coma/respiratory failure.
• EVACUATE; if descent temporarily blocked, maximize O2 + Gamow + drugs and descend the instant feasible.
• PREVENTION (when timeline allows): graded ascent (≤500 m/day sleeping gain >3,000 m, rest day q1,000 m), acetazolamide 125 mg BID prophylaxis; nifedipine for HAPE-prone.

Clinical Pearls

• Ataxia + altered mentation = HACE; dyspnea at rest + frothy sputum + hypoxia = HAPE — both are emergencies.
• DESCENT is the definitive treatment for both — even ~1,000 m helps; don't delay it for drugs.
• HACE drug = dexamethasone; HAPE drug = nifedipine; oxygen + Gamow bag bridge when descent is blocked.
• Acetazolamide is for AMS prophylaxis/treatment and HACE adjunct, not the primary for established HACE/HAPE.
• Prevent with graded ascent (≤500 m/day sleeping gain >3,000 m) and acetazolamide prophylaxis (WMS).
• Africa has the terrain (Kilimanjaro, Ethiopian highlands) — altitude illness is a real AFRICOM environmental threat.

Character Development

Patient. A partner-force soldier from a pastoralist family in the Horn of Africa who has drunk unpasteurized camel/goat milk and helped with birthing livestock. He presents with weeks of drenching, fluctuating ('undulant') fevers, night sweats, profound fatigue, joint and low-back pain, and now testicular swelling.

Medic. SFC Marcus “Herdsman” Bello, 36 — 18D who knows that in pastoralist Africa a chronic relapsing fever with sweats, big joints, and an animal/raw-milk history is brucellosis until proven otherwise, and that the drug choice has a TB twist.

Environment

Before. The Horn of Africa livestock belt, where Brucella is endemic in goats, sheep, cattle, and camels, and raw-milk consumption and assisting at births are everyday exposures. Blood culture and serology are reachable through partner-nation/NGO labs; TB is heavily co-endemic.

During. Bello pieces together the undulant fever, sweats, sacroiliac/back pain, fatigue out of proportion, and epididymo-orchitis with the raw-milk and birthing exposure — the classic brucellosis syndrome — and recognizes this is a prolonged-combination-antibiotic, refer-and-treat problem, not a single-shot fix.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• SUSPECT from exposure + pattern: raw milk/livestock birthing + undulant fever + sweats + arthralgia/sacroiliitis + orchitis.
• DIAGNOSE: serology + blood culture — WARN THE LAB (Brucella is hazardous/lab-acquired-infection risk).
• TREAT (prolonged combination): doxycycline 100 mg BID x6 wk + streptomycin/gentamicin x2–3 wk (lowest relapse).
• AVOID doxycycline-rifampin where TB is co-endemic — protects against rifampin-resistant TB.
• SCREEN for focal disease: endocarditis (murmur → echo; #1 cause of death), spondylitis, neurobrucellosis; longer triple therapy if present.
• REFER for the weeks-long course; flag pregnancy (miscarriage risk).
• PREVENT: no unpasteurized dairy; PPE around livestock births/slaughter; team awareness (aerosol/lab hazard).

Clinical Pearls

• Brucellosis = undulant fever + night sweats + fatigue + arthralgia/sacroiliitis + orchitis, after raw milk/livestock exposure.
• Treat with PROLONGED COMBINATION therapy — doxycycline x6 wk + aminoglycoside (streptomycin/gentamicin) x2–3 wk has the lowest relapse.
• Avoid doxycycline-rifampin in TB-co-endemic regions — protects against rifampin-resistant TB.
• Endocarditis is rare but the #1 cause of death — check for a murmur; spondylitis/neurobrucellosis need longer therapy.
• Warn the lab — Brucella is a lab-acquired-infection hazard and a potential aerosol bioagent.
• Prevention is raw-milk avoidance and PPE around births/slaughter — a One-Health, partner-force message.

Character Development

Patient. SSG 'Wader' Okonkwo, 29 — a SOF soldier who waded through flooded, muddy water during a riverine operation in coastal East Africa ~10 days ago. After abrupt fever, severe calf myalgias, and headache, he now has jaundice, decreasing urine output, and conjunctival redness (suffusion).

Medic. SFC Talia “Torrent” Mensah, 35 — 18D who connects fresh-water/flood exposure, killer calf pain, conjunctival suffusion, and now jaundice + renal failure to Weil's disease, and knows doxycycline does double duty in this region.

Environment

Before. Coastal/riverine East Africa after seasonal flooding — Leptospira from rodent urine contaminates standing water, and wading/immersion with skin abrasions is the classic exposure. Rickettsial illness is also endemic, which matters for drug choice.

During. Mensah recognizes the biphasic illness tipping into the severe icteric phase: jaundice, oliguric AKI, conjunctival suffusion, and risk of pulmonary hemorrhage — Weil's syndrome, which can deteriorate fast and carries a real case-fatality rate.

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Vital Signs

Physical Examination

Critical Actions

• SUSPECT from exposure + pattern: floodwater/mud immersion + severe calf myalgia + conjunctival suffusion + fever.
• RECOGNIZE WEIL'S (severe): jaundice + AKI + hemorrhage (± pulmonary hemorrhage) — 5–15% CFR; evacuate.
• TREAT EARLY (don't wait for confirmation): mild — doxycycline 100 mg BID x7 d; severe — IV penicillin G or ceftriaxone 1–2 g daily.
• EMPIRIC DOXYCYCLINE also covers rickettsial mimics (penicillin/cephalosporins do NOT) — smart when undifferentiated.
• SUPPORTIVE: fluids for shock, manage AKI (dialysis at higher level), O2 + airway readiness for pulmonary hemorrhage, correct coagulopathy.
• TEST/TREAT malaria in parallel (co-endemic, overlapping).
• WATCH for Jarisch-Herxheimer after first antibiotic dose.
• PREVENT: avoid stagnant-water wading, cover abrasions; consider doxycycline prophylaxis for high-risk immersion.

Clinical Pearls

• Leptospirosis: floodwater/mud immersion + severe calf myalgia + conjunctival suffusion + fever — biphasic course.
• Weil's disease (severe) = jaundice + AKI + hemorrhage; pulmonary hemorrhage is the high-mortality complication.
• Treat early: doxycycline (mild) or IV penicillin G/ceftriaxone (severe) — don't await confirmation.
• Empiric doxycycline also covers endemic rickettsial disease — penicillin/cephalosporins do not.
• Support the kidneys (dialysis at higher care) and lungs — organ failure is often reversible; evacuate.
• Co-endemic malaria mimics/coexists — test and treat in parallel; cover abrasions and avoid stagnant water.

Character Development

Patient. A partner-force candidate (and, in parallel, a U.S. trainee with sickle cell trait) during an arduous selection event in the heat. He collapses late in a hard effort — not with the classic stagger of heat stroke, but with severe muscle pain, weakness, and dark 'cola-colored' urine, and is found to be acidotic.

Medic. SFC Grace “Cadence” Idris, 36 — 18D who knows the modern, evidence-updated story of sickle cell trait: it is NOT a death sentence under good precautions, but it IS a real risk factor for exertional rhabdomyolysis — and the killers are rhabdo, hyperkalemia, and heat.

Environment

Before. A grueling selection/assessment in heat. Sickle cell trait is common in the African and African-diaspora population, and exertional collapse during intense, sustained effort — especially with dehydration, heat, and no rest — is the danger window.

During. Idris faces exertional collapse with marked myalgia, weakness, and tea-/cola-colored urine — rhabdomyolysis — and must distinguish it from (and manage alongside) heat illness, guard against hyperkalemia and acute kidney injury, and resist outdated fatalism about the trait.

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Vital Signs

Physical Examination

Critical Actions

• HOLD THE MODERN VIEW: SCT is NOT a death sentence under good precautions, but IS a real exertional-rhabdomyolysis risk factor (Army cohort).
• RECOGNIZE RHABDO: muscle pain/weakness + cola-colored urine (myoglobinuria) + acidosis after hard exertion.
• AGGRESSIVE IV FLUIDS early, titrated to urine output — the single most important intervention (protects kidneys, flushes myoglobin).
• MANAGE HYPERKALEMIA (the acute killer): ECG monitoring; calcium (membrane), insulin+dextrose (shift), resins/dialysis (remove).
• CHECK RECTAL TEMP — differentiate/co-manage exertional heat stroke (>40°C + CNS → immediate cooling); the two can coexist.
• STOP exertion; cool if heat involved; evacuate (AKI may need dialysis).
• PREVENT with UNIVERSAL exertional-injury precautions: acclimatization, hydration, work-rest, no untrained max efforts.

Clinical Pearls

• Modern evidence (Army cohort, ~48,000): SCT is NOT linked to higher death under good precautions, but IS linked to higher exertional rhabdomyolysis.
• Rhabdo = muscle pain/weakness + cola-colored urine + acidosis — aggressive early IV fluids are the key intervention.
• Hyperkalemia is the acute killer: calcium (stabilize) → insulin+dextrose (shift) → resins/dialysis (remove); watch the ECG.
• Check a RECTAL temp — distinguish/co-manage exertional heat stroke (>40°C + CNS → cool first).
• Universal exertional-injury precautions (acclimatization, hydration, work-rest) protect everyone and neutralized the excess risk in the data.
• Don't fatalistically stigmatize trait carriers — recognize the real (rhabdo) risk and train smart.

Character Development

Patient. SGT 'Camel' Diallo, 26 — a conscientious soldier on a long, hot movement who has been drinking water constantly to 'stay ahead of dehydration.' Late in the event he becomes confused, nauseated, and headachy, then has a seizure — with a near-normal core temperature and a recent history of frequent urination and weight GAIN.

Medic. SFC Owen “Electrolyte” Park, 35 — 18D who knows the deadliest mistake here is the intuitive one: pouring more hypotonic fluid into a collapsed, confused soldier who is actually water-INTOXICATED, not dehydrated.

Environment

Before. A prolonged, hot endurance movement where overzealous plain-water intake is common. Exercise-associated hyponatremia (EAH) classically strikes the careful hydrator who overdrinks during sustained exertion, diluting serum sodium dangerously.

During. Park confronts an altered, seizing soldier and the critical fork: is this heat stroke, dehydration, or hyponatremia? The history (constant drinking, weight gain), the near-normal rectal temperature, and the encephalopathy point to severe EAH — where giving more hypotonic fluid could kill him and hypertonic saline is the treatment.

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Vital Signs

Physical Examination

Critical Actions

• DO NOT push hypotonic/large isotonic fluids into a confused, collapsed soldier until you've excluded EAH — it can be lethal.
• DIFFERENTIATE with a RECTAL TEMP: heat stroke >40°C + CNS; EAH near-normal temp + CNS; plus history (overdrinking + weight GAIN = EAH).
• SEVERE EAH (seizure/encephalopathy): 100 mL bolus 3% hypertonic saline IV, repeat q10 min up to 3 doses (raise Na ~4–5 mmol/L); protect airway, control seizure.
• MILD EAH: fluid restriction until urination + oral salt (broth/salty snacks); observe ≥1 h (gut water can still absorb).
• CHECK GLUCOSE; consider point-of-care sodium if available.
• EVACUATE severe cases; continue to monitor mentation.
• PREVENT: drink to THIRST (not maximal), include sodium on long hot efforts; counter 'overdrink to beat dehydration' dogma.

Clinical Pearls

• EAH is dilutional — too much water, too little sodium; more hypotonic fluid WORSENS the cerebral edema. Don't reflexively push fluids.
• Differentiate with a RECTAL temp (heat stroke >40°C) and history (EAH = overdrinking + weight GAIN; dehydration = weight loss/thirst) — treatments are OPPOSITE.
• Severe symptomatic EAH: 100 mL boluses of 3% hypertonic saline q10 min x3 (raise Na ~4–5 mmol/L) — WMS guidance.
• Mild EAH: fluid restriction + oral salt; observe ≥1 h (gut water still absorbs after stopping).
• Prevent by drinking to THIRST with sodium — 'overdrink to beat dehydration' dogma CAUSES EAH.
• The conscientious heavy drinker is the classic EAH victim — the counterintuitive killer among exertional collapses.

Character Development

Patient. SSG 'Ranger' Mwangi, 31 — bitten on the hand while clearing a structure at night in rural Tanzania; the snake was long, fast, and slate-colored (a black mamba). Within 30 minutes he has drooping eyelids, slurred speech, difficulty swallowing, and now labored breathing — with minimal local swelling.

Medic. SFC Ravi “Anchor” Nair, 36 — 18D who knows the neurotoxic-elapid bite is the mirror image of the viper bite: little local damage but a descending paralysis that kills by respiratory failure — and that here, unlike the viper, pressure immobilization is INDICATED and ventilation may be the lifesaving therapy.

Environment

Before. Rural Tanzania at night — black mamba and cobra country. Neurotoxic elapid venom blocks neuromuscular transmission, producing a descending paralysis (eyes → bulbar → respiratory muscles). Antivenom (SAIMR polyvalent) is hours away; the team has a BVM and a definitive airway kit but limited ventilator capacity.

During. Nair watches a classic descending paralysis march: ptosis and ophthalmoplegia, then bulbar signs (slurred speech, drooling, dysphagia), then failing respiratory muscles — a patient who may need to be ventilated by hand for hours until antivenom and recovery, with almost no local wound to show for a lethal envenomation.

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Vital Signs

Physical Examination

Critical Actions

• IDENTIFY NEUROTOXIC SYNDROME: rapid descending paralysis (ptosis → bulbar → respiratory) with MINIMAL local injury.
• APPLY PRESSURE-IMMOBILIZATION (indicated for neurotoxic elapid bite WITHOUT local necrosis — opposite of viper bite).
• AIRWAY + ASSISTED VENTILATION is the lifesaver: support with BVM early, secure a definitive airway, ventilate — a ventilated paralyzed patient survives.
• PROLONGED VENTILATION: rotate providers, monitor SpO2 + capnography, sedate/analgese the intubated patient, eye care/positioning, document trajectory.
• ANTIVENOM (definitive): regional polyvalent (SAIMR); prep for anaphylaxis (epinephrine/fluids/airway).
• ANTICHOLINESTERASE TRIAL (atropine + neostigmine) — adjunct, more useful for post-synaptic (cobra) than pre-synaptic (mamba) toxins.
• DON'T be fooled by a benign-looking wound; no cutting/sucking/ice/arterial tourniquet; tetanus update.
• EVACUATE emergently to ventilator/ICU capability; be prepared to breathe for them the whole way.

Clinical Pearls

• Neurotoxic elapid (mamba/cobra) bite: descending paralysis (ptosis → bulbar → respiratory) with MINIMAL local injury — mirror image of the viper bite.
• Pressure-immobilization IS indicated for neurotoxic bites without local necrosis (opposite of cytotoxic viper bites).
• The killer is respiratory paralysis — assisted ventilation keeps a paralyzed patient alive; a ventilated patient survives until antivenom works.
• It's a prolonged-care problem: be ready to hand-ventilate for hours — rotate providers, monitor, sedate, evacuate.
• Antivenom is definitive (prep for anaphylaxis); anticholinesterase (atropine+neostigmine) is an adjunct, better for cobra (post-synaptic) than mamba (pre-synaptic).
• A benign-looking wound does NOT mean mild envenomation in an elapid bite — don't be fooled.

Character Development

Patient. SGT 'Tripwire' Adeyemi, 27 — takes fragmentation from a command-detonated IED during a vehicle interdiction in Somalia, with a high-and-deep wound at the right groin (inguinal crease) pumping bright-red blood. A limb tourniquet placed above it does nothing — the bleeding is too proximal.

Medic. SFC Dana “Tourniquet” Cole, 35 — 18D who knows the junctional zones (groin, axilla, neck base) are where standard tourniquets fail, and that this is now a wound-packing + junctional-device + whole-blood problem against the clock.

Environment

Before. A dismounted interdiction in Somalia; an IED strike produces a junctional groin wound. Care under fire transitions to tactical field care behind cover. The element carries hemostatic gauze, a junctional tourniquet, TXA, and a walking-blood-bank capability.

During. Cole confronts catastrophic junctional hemorrhage — too proximal for a limb tourniquet — and must pack the wound with hemostatic gauze, apply a junctional tourniquet, and treat the hemorrhagic shock with whole blood, all while keeping the MARCH sequence and the tactical situation in mind.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE junctional bleed: inguinal/axillary/neck-base, pulsatile, limb tourniquet INEFFECTIVE (too proximal).
• PACK aggressively with CoTCCC hemostatic gauze deep onto the vessel; firm pressure ~3 min.
• APPLY a JUNCTIONAL TOURNIQUET device for sustained proximal compression.
• WHOLE BLOOD (LTOWB) is resuscitation fluid of choice — walking blood bank (ROLO/Valkyrie); minimize crystalloid; give calcium.
• TXA 2 g IV/IO single dose (3-h window removed; earlier better).
• PERMISSIVE HYPOTENSION (radial pulse / SBP ~100) until hemorrhage controlled.
• MARCH sweep: reassess airway, chest (tension pneumo), circulation, prevent HYPOTHERMIA (lethal triad).
• Ceftriaxone 2 g (Change 25-1) for open wound; ketamine analgesia; TCCC card; EVACUATE to surgery.

Clinical Pearls

• Limb tourniquets fail on junctional (groin/axilla/neck) bleeds — pack with hemostatic gauze + apply a junctional tourniquet device.
• Whole blood (LTOWB, walking blood bank) is the resuscitation fluid of choice — minimize crystalloid; give calcium.
• TXA is now a single 2 g IV/IO dose; the 3-hour window is removed (benefit out to ~12 h, earlier better).
• Permissive hypotension (radial pulse / SBP ~100) until hemorrhage is controlled.
• Fight the lethal triad — hypothermia, acidosis, coagulopathy — with warming, blood not crystalloid, and calcium.
• Junctional/truncal hemorrhage is now a leading preventable death as limb-tourniquet use has matured — train for the bleeds the tourniquet can't reach.

Character Development

Patient. SSG 'Reed' Calloway, 30 — sustained a penetrating chest wound from small-arms fire to the right anterior chest. After a vented chest seal is placed, he becomes increasingly dyspneic, agitated, and hypotensive, with absent right-sided breath sounds and distended neck veins.

Medic. SFC Owen “Bellows” Reilly, 35 — 18D who knows a deteriorating penetrating-chest casualty with progressive respiratory distress and shock is a tension pneumothorax until proven otherwise — and that current TCCC gives two needle sites and a finger-thoracostomy fallback.

Environment

Before. A firefight with a penetrating chest wound; a vented chest seal was applied. Progressive tension physiology develops as air accumulates under pressure. The element has 14-ga 3.25-inch decompression needles and providers trained in finger thoracostomy.

During. Reilly recognizes the lethal triad of tension pneumothorax — worsening respiratory distress, hypotension, and absent unilateral breath sounds — and must decompress decisively, knowing where the needle goes, how many attempts, and what to do if the needle fails.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• RECOGNIZE: progressive dyspnea + hypotension + absent unilateral breath sounds (± JVD) after chest trauma = tension pneumothorax.
• NEEDLE DECOMPRESS: 14-ga 3.25-in (83 mm), at 5th ICS anterior axillary line OR 2nd ICS midclavicular line, over the top of the rib, perpendicular; hold 5–10 s.
• Max TWO needle attempts; leave catheter, remove needle.
• IF NEEDLE FAILS → FINGER THORACOSTOMY (4th/5th ICS AAL) if trained/in scope — more reliable; progresses to chest tube in prolonged care.
• CHECK the vented chest seal — an occluded seal can cause tension; burp/replace.
• REASSESS breath sounds/hemodynamics (improvement confirms Dx); anticipate recurrence — monitor and re-decompress as needed.
• Continue MARCH (hemorrhage, other injuries); oxygen/ventilatory support; analgesia; prevent hypothermia.
• EVACUATE — needs chest tube / surgical capability.

Clinical Pearls

• Tension pneumothorax: progressive distress + hypotension + absent unilateral breath sounds; tracheal deviation/JVD are late/unreliable.
• Decompress with a 14-ga 3.25-in (83 mm) needle at 5th ICS AAL OR 2nd ICS MCL, over the top of the rib; max two attempts.
• 2nd ICS MCL fails more (chest-wall thickness); lateral site is reliable but mind depth (cardiac/vessel risk if hubbed).
• Needle fails → finger thoracostomy (if trained) — more reliable; chest tube in prolonged care.
• An occluded vented chest seal can CAUSE tension — burp/replace it.
• Anticipate recurrence (catheter clots/kinks) — monitor and re-decompress; evacuate to surgical capability.

Character Development

Patient. SGT 'Ledger' Park, 26 — multiple gunshot wounds to the thigh and abdomen during a raid in the Sahel, with controlled extremity hemorrhage (tourniquet) but ongoing non-compressible abdominal bleeding. He is pale, cold, confused, with a thready pulse — Class IV hemorrhagic shock far from any blood bank.

Medic. MSG Dolores “Type-O” Park, 39 — senior 18D who runs a walking blood bank as routinely as she runs an IV, and who knows that in deep hemorrhagic shock the answer is blood — ideally fresh whole blood from the team — not bags of crystalloid.

Environment

Before. A raid deep in the Sahel, hours from surgical care, with non-compressible truncal hemorrhage that the medic cannot fix in the field. The element has a prescreened low-titer group O donor roster (ROLO-style), field collection kits, TXA, and calcium.

During. Park has controlled what she can (tourniquet) but faces ongoing abdominal bleeding she can't compress, and a casualty crashing into profound shock. Damage-control resuscitation with whole blood, permissive hypotension, TXA, calcium, and warming — while racing to surgery — is the only bridge.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• BLOOD, NOT CRYSTALLOID: low-titer group O whole blood (LTOWB) is the resuscitation fluid of choice — activate the walking blood bank (ROLO/Valkyrie).
• DCR: minimize crystalloid; whole blood or 1:1:1; warm everything.
• PERMISSIVE HYPOTENSION to radial pulse / SBP ~100 (but ~100–110 if significant TBI).
• TXA 2 g IV/IO single dose early (3-h window removed).
• CALCIUM early and with transfusion (shock + citrate → hypocalcemia impairs clotting/cardiac function).
• FIGHT THE LETHAL TRIAD: aggressive hypothermia prevention, blood, TXA.
• RESUSCITATE TO CLINICAL ENDPOINTS (radial pulse, mentation, trend) — no lab needed; reassess hemorrhage control repeatedly.
• EVACUATE emergently — non-compressible truncal hemorrhage needs a surgeon; you are buying time.

Clinical Pearls

• Low-titer group O whole blood (LTOWB) is the resuscitation fluid of choice — a walking blood bank (ROLO/Valkyrie) turns the team into the blood supply.
• Damage-control resuscitation: blood not crystalloid, permissive hypotension (radial pulse/SBP ~100), fight the lethal triad, give calcium.
• Permissive hypotension target rises to SBP ~100–110 with significant TBI (the injured brain hates hypotension).
• TXA 2 g IV/IO single dose early (window removed); calcium early and with transfusion.
• Resuscitate to clinical endpoints — radial pulse and mentation/trend — when you have no lab.
• You can't fix non-compressible truncal hemorrhage in the field — DCR buys time to the surgeon; evacuate.

Character Development

Patient. SGT 'Mason' Okafor, 28 — severe maxillofacial trauma from an IED fragment that shattered the mandible and midface, with heavy oral bleeding, broken teeth, and progressive difficulty maintaining his own airway. He is conscious but struggling, leaning forward and spitting blood.

Medic. SFC Aimee “Patency” Okafor, 34 — 18D who knows the updated TCCC airway doctrine (Change 24-1): positioning first, the surgical airway is the definitive battlefield answer for destroyed-face anatomy, and supraglottic airways are no longer part of tactical field care.

Environment

Before. A blast injury producing massive maxillofacial trauma. The face is too disrupted for ordinary adjuncts, and blood/secretions threaten the airway. The element has a surgical-airway kit and providers trained in cricothyroidotomy.

During. Okafor faces a threatened airway from facial destruction and bleeding — the kind of anatomy where bag-mask and supraglottic devices fail — and must decide between aggressive positioning/suction and moving to a surgical cricothyroidotomy before the airway is lost.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• MASSIVE HEMORRHAGE first (MARCH) — control catastrophic oral/facial bleeding; suction.
• POSITION the conscious casualty to protect his own airway (sit up / lean forward); suction aggressively — do NOT force supine.
• NPA in the respiration assessment per Change 24-1; SUPRAGLOTTIC AIRWAYS are NOT in tactical field care.
• RECOGNIZE that BVM/SGA fail on destroyed facial anatomy — plan from BELOW the obstruction.
• SURGICAL CRICOTHYROIDOTOMY when airway is failing/lost — act BEFORE complete obstruction; cuffed tube, confirm placement, secure.
• ANALGESIA/SEDATION (ketamine) to facilitate the procedure in a conscious patient.
• REASSESS mentation continuously (tiring/obtunding = imminent airway loss); manage associated blast injuries (TBI, neck, eye).
• Oxygen/ventilatory support after securing; prevent hypothermia; TCCC card; EVACUATE.

Clinical Pearls

• TCCC Change 24-1: positioning first, NPA in the Respiration assessment, supraglottic airways REMOVED from tactical field care.
• Let a conscious maxillofacial casualty sit up/lean forward to protect his airway — don't force supine; suction aggressively.
• BVM and SGAs fail on destroyed facial anatomy — the definitive battlefield airway comes from below: surgical cricothyroidotomy.
• Do the surgical airway BEFORE complete obstruction/arrest — a tiring, obtunding facial-trauma patient is about to lose the airway.
• Use ketamine to facilitate the surgical airway in a conscious patient (preserves drive/reflexes relatively well).
• MARCH still applies — control massive oral hemorrhage first; reassess for TBI and associated blast injuries.

Character Development

Patient. SGT 'Ridge' Bello, 29 — close to a large IED blast during a route-clearance mission in Mali. Initially 'dazed but walking,' over the next hour he becomes confused, then has a decreasing level of consciousness with a blown right pupil and rising blood pressure with a slowing heart rate.

Medic. SFC Marcus “Mentation” Bello, 36 — 18D who knows that in TBI the two things that turn a survivable brain injury into a fatal one are HYPOXIA and HYPOTENSION, and that the rules for blood-pressure targets flip compared to a pure hemorrhage casualty.

Environment

Before. A route-clearance mission with a large IED blast — primary blast and blunt mechanisms for TBI. The casualty is hours from neurosurgical care. The element has whole blood, TXA, hypertonic saline, and the ability to monitor and reassess mentation over time.

During. Bello watches a classic deterioration — a lucid interval giving way to declining consciousness, an unequal/blown pupil, and Cushing's response (hypertension + bradycardia) — signs of rising intracranial pressure and herniation, demanding the brain-protective bundle and urgent evacuation.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• AVOID HYPOXIA (SpO2 >90%) and AVOID HYPOTENSION — the two sins that worsen TBI; ventilate at a NORMAL rate (avoid hyper-/hypocarbia).
• BP TARGET IS HIGHER for significant TBI: SBP ~100–110 (resuscitate to this, not to permissive hypotension, if also bleeding).
• TXA 2 g IV/IO (significant TBI is an indication; CRASH-3).
• HERNIATION (blown pupil/Cushing's triad): head up ~30° + midline, hypertonic saline (3% bolus), optimize oxygenation/ventilation; mild hyperventilation ONLY as last-ditch for active herniation.
• PREVENT seizures, shivering, hyperthermia, pain/agitation (all raise ICP).
• SERIAL mentation/pupil/motor exams — treat any decline as expanding lesion ('talk and die' lucid interval).
• MARCH sweep for hemorrhage/other blast injuries; secure airway as LOC falls.
• EVACUATE emergently to neurosurgery; teleconsult; document trend on TCCC card.

Clinical Pearls

• Hypoxia and hypotension are the two sins that turn survivable TBI fatal — keep SpO2 >90% and pressure up; ventilate at a normal rate.
• BP target FLIPS for significant TBI: aim SBP ~100–110 (higher than permissive hypotension) — the injured brain needs perfusion.
• TXA 2 g is indicated for significant TBI (CRASH-3); give early.
• Herniation (blown pupil + Cushing's triad): head up/midline, hypertonic saline, optimize ventilation; mild hyperventilation only as last-ditch.
• Reassess mentation serially — the lucid interval ('talk and die') means a single normal exam is falsely reassuring.
• Delayed evacuation makes TBI a prolonged neurocritical-care problem — sustain brain-protective physiology over hours.

Character Development

Patient. SSG 'Forge' Diallo, 31 — caught in a vehicle fuel fire after an IED strike in Chad, with deep burns across the anterior torso, both arms, and face. He has singed nasal hair, a hoarse voice, carbonaceous sputum, and was in an enclosed cab — raising alarm for inhalation injury.

Medic. SFC Lena “Flashpoint” Brooks, 35 — 18D who knows that with burns the early killers are the AIRWAY (inhalation injury swells shut) and that the long game is fluid resuscitation done with DISCIPLINE — too little or too much both harm — using the Rule of Tens and a flow sheet.

Environment

Before. A vehicle fuel fire from an IED strike; the casualty was briefly enclosed in the cab with smoke. Burns plus probable inhalation injury, hours from a burn-capable facility. The element has Ringer's lactate, airway equipment, and a burn flow sheet.

During. Brooks weighs the urgent airway threat (inhalation injury that may swell the airway shut within hours — secure it EARLY) against starting calculated fluid resuscitation, estimating TBSA, preventing hypothermia, and avoiding the over-resuscitation 'fluid creep' that kills burn patients.

OPQRST

Vital Signs

Physical Examination

Critical Actions

• AIRWAY FIRST if inhalation injury suspected (facial burns, hoarse voice, soot, carbonaceous sputum, enclosed fire) — secure a DEFINITIVE airway EARLY before edema closes it.
• HIGH-FLOW OXYGEN empirically (CO makes SpO2 falsely normal); suspect CO/cyanide with altered mentation/acidosis.
• ESTIMATE %TBSA (Rule of Nines; palm ≈1%) — count only partial/full-thickness.
• START FLUIDS by Rule of Tens: %TBSA × 10 = mL/hr LR (+100 mL/hr per 10 kg >80 kg); Modified Brooke (2 mL/kg/%TBSA) preferred over Parkland.
• TITRATE TO URINE OUTPUT (~30–50 mL/hr adult; 0.5–1 mL/kg/hr) on the JTS Burn Flow Sheet — avoid 'fluid creep'/over-resuscitation.
• PREVENT HYPOTHERMIA aggressively (warm patient + fluids; dry clean dressings; brief cooling of burn only).
• WATCH circumferential burns (compartment/escharotomy need) and sweep for blast trauma.
• PAIN control (ketamine/opioids); teleconsult burn specialist; EVACUATE to burn-capable care.

Clinical Pearls

• Inhalation injury (facial burns, hoarse voice, soot, carbonaceous sputum, enclosed fire) → secure the airway EARLY, before it swells shut.
• Estimate %TBSA (Rule of Nines), start fluids by Rule of Tens (%TBSA × 10 = mL/hr LR), Modified Brooke preferred over Parkland.
• TITRATE to urine output (~30–50 mL/hr) on the JTS Burn Flow Sheet — avoid 'fluid creep'/over-resuscitation, which kills.
• Enclosed smoke = CO/cyanide risk; SpO2 reads falsely normal — give high-flow O2 empirically.
• Burns lose heat fast — prevent hypothermia aggressively (warm patient + fluids); watch circumferential burns for escharotomy.
• Delayed evacuation makes burns a prolonged-care problem — sustained titrated fluids, airway, pain, wound care, nutrition.

Character Development

Patient. SGT 'Anvil' Okonkwo, 27 — dismounted when a buried IED detonated, causing a traumatic above-knee amputation of the left leg and a suspected unstable pelvic fracture (pain, instability, scrotal/flank bruising). He is in profound shock with the classic blast-injury pattern.

Medic. SFC Talia “Keystone” Mensah, 35 — 18D who knows the dismounted-blast triad (amputation + pelvic fracture + perineal injury) is a massive-hemorrhage emergency where a tourniquet handles the limb but the PELVIS is a hidden reservoir that needs a binder and blood.

Environment

Before. A dismounted patrol over a buried IED — the mechanism for the devastating 'dismounted complex blast injury' pattern (bilateral/unilateral amputations, pelvic and perineal trauma). Hours from surgery. The element has tourniquets, a pelvic binder, hemostatic gauze, and a walking blood bank.

During. Mensah controls the amputation hemorrhage with a tourniquet but recognizes the unstable pelvis as a major occult bleeding source — the pelvic ring can hold liters — requiring a binder, aggressive blood-based resuscitation, and packing of any junctional/perineal wounds.

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Vital Signs

Physical Examination

Critical Actions

• MARCH — control ALL hemorrhage sources: TOURNIQUET high on the amputation stump (second TQ if needed).
• PELVIC BINDER over the GREATER TROCHANTERS for the unstable pelvis (occult hemorrhage) — internally rotate/bind legs; do NOT spring/rock the pelvis.
• PACK perineal/junctional wounds with hemostatic gauze; junctional device if needed.
• WHOLE BLOOD (walking blood bank) + TXA 2 g + calcium; permissive hypotension (SBP ~100; ~100–110 if TBI); prevent hypothermia.
• FULL SWEEP for associated injuries: other amputations, GU/perineal, intra-abdominal, TBI, blast lung/ear.
• ANTIBIOTICS (ceftriaxone 2 g, Change 25-1) for heavily contaminated open wounds (invasive-infection risk).
• KETAMINE analgesia (shock-safe); reassess all hemorrhage control repeatedly; TCCC card.
• EVACUATE emergently — unstable pelvis/complex blast needs surgical + angiographic control.

Clinical Pearls

• An unstable pelvic fracture bleeds LITERS occultly — apply a pelvic binder over the GREATER TROCHANTERS; don't spring/rock the pelvis.
• Dismounted complex blast = amputation + pelvic + perineal trauma — controlling the obvious amputation is NOT controlling all the bleeding.
• Layer hemorrhage control: stump tourniquet + pelvic binder + perineal/junctional packing + whole-blood DCR (TXA, calcium).
• Sweep for the hidden injuries: second amputation, GU/perineal, intra-abdominal, TBI, blast lung/ear.
• Heavily contaminated perineal/pelvic wounds = high infection (incl. invasive fungal) risk — early ceftriaxone 2 g.
• Ketamine is the shock-safe analgesic; bridge with DCR to surgical/angiographic control.

Character Development

Patient. Three casualties from a single contact in Niger: (A) a soldier with a painful but minor shrapnel forearm wound, still able to fight; (B) a soldier with a closed femur fracture, in severe pain but hemodynamically stable; and (C) a soldier in hemorrhagic shock from a junctional wound, in agony, requiring a painful intervention.

Medic. SFC Owen “Triad” Reilly, 35 — 18D who applies the TCCC triple-option analgesia framework like a decision tree: the right drug depends on the casualty's pain, their mission ability, and — critically — whether they're in shock or respiratory distress.

Environment

Before. A multi-casualty contact in Niger with three soldiers needing pain control across the spectrum — mild, severe-but-stable, and severe-with-shock. The element carries the combat wound medication pack (meloxicam + acetaminophen), oral transmucosal fentanyl citrate (OTFC), and ketamine.

During. Reilly must rapidly match each casualty to the correct TCCC analgesia option — avoiding the dangerous error of giving a respiratory-depressant opioid to the shocked casualty — while keeping the able-bodied soldier in the fight and controlling severe pain safely.

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Vital Signs

Physical Examination

Critical Actions

• MARCH FIRST — control massive hemorrhage and airway before analgesia; pain control never precedes life-threats.
• OPTION 1 (mild pain, still able to fight): Combat Wound Medication Pack — meloxicam + acetaminophen (no sedation/respiratory depression).
• OPTION 2 (moderate-severe, NO shock/respiratory distress): OTFC (oral transmucosal fentanyl) — monitor RR/sedation/BP; naloxone available; tape lozenge to finger.
• OPTION 3 (moderate-severe WITH shock/respiratory distress, or painful procedure): KETAMINE — maintains BP/respiratory drive; give slowly; manage emergence/secretions.
• DO NOT give respiratory-depressant opioids to a casualty in shock or respiratory distress — the key safety rule.
• TITRATE and REASSESS pain + vitals frequently; re-dose as needed.
• DOCUMENT drug/dose/time on the TCCC card; continue MARCH care.
• PROLONGED CARE: sustain analgesia/sedation, watch for delirium and respiratory depression over time.

Clinical Pearls

• TCCC triple-option analgesia: (1) mild + still fighting → meloxicam + acetaminophen; (2) moderate-severe, no shock/resp distress → OTFC; (3) moderate-severe WITH shock/resp distress or procedure → ketamine.
• Ketamine is the analgesic of choice in shock — maintains BP and respiratory drive; opioids depress both and are dangerous in shock.
• Keep the mission-capable, mildly injured soldier in the fight with the non-sedating combat wound medication pack.
• OTFC needs monitoring (RR, sedation, BP), naloxone available, lozenge taped to finger; ketamine: give slowly, manage emergence/secretions.
• Analgesia never precedes MARCH life-threats — hemorrhage and airway first.
• In prolonged care, analgesia/sedation becomes an ongoing balance — sustain control, avoid respiratory depression, watch for delirium.

Character Development

Patient. SGT 'Hold' Adeyemi, 28 — stabilized after a gunshot wound to the thigh (tourniquet converted to a packed wound) during a deep operation in the Sahel, now facing a 24- to 48-hour delay to surgical care because evacuation is grounded by weather and threat.

Medic. SFC Dana “Anchor” Cole, 35 — 18D who knows the hardest part of SOF medicine isn't the first ten minutes of TCCC but the next ten HOURS — holding a casualty alive with limited resources until evacuation, using the MARC²H³-PAWS-L framework and tiered austere standards.

Environment

Before. A deep Sahel operation with a long, uncertain evacuation timeline (‘no/low/slow’ evacuation). The casualty is past the acute TCCC phase but far from surgery — the definition of prolonged casualty care. Resources: limited blood, a casualty card, teleconsult capability, and the team's hands and discipline.

During. Cole shifts mental models from the fast, algorithmic life-saving of TCCC to the slow, sustained, nursing-and-monitoring discipline of PCC — anticipating problems over hours, documenting trends, tiering care to what she actually has, and planning the evacuation she doesn't yet have.

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Vital Signs

Physical Examination

Critical Actions

• SHIFT MINDSET TCCC→PCC: from fast life-threat control to sustained, anticipatory, trend-driven nursing care.
• ASSESS/REASSESS with MARC²H³-PAWS-L (Massive hemorrhage, Airway, Respiration, Circulation+Calcium, Hypothermia/Head/Hypotension, Pain, Antibiotics, Wounds, Splinting, Litter/Logistics/teLemedicine).
• RESOURCE BY TIER: deliver minimum / better / best per what you actually have; improvise upward.
• PLAN MOVEMENT with Ruck-Truck-House-Plane — match care to setting; aim toward evacuation.
• RE-SURVEY for missed/occult injuries (secondary + tertiary exam).
• ESTABLISH monitoring + DOCUMENTATION rhythm (vital trends, urine output, mentation, wounds on the PCC casualty card).
• SET UP warming, positioning, fluids/blood, analgesia/sedation, wound antibiotics.
• INITIATE TELECONSULT EARLY and build the evacuation request/contingency now.

Clinical Pearls

• PCC begins when evacuation is delayed — the mindset shifts from fast TCCC life-threat control to sustained, anticipatory, trend-driven care.
• Use MARC²H³-PAWS-L for structured, repeated whole-patient reassessment over time (not the one-pass MARCH).
• Resource by minimum/better/best — deliver the best care possible WITH WHAT YOU HAVE; improvise upward.
• Ruck-Truck-House-Plane: match care and movement to setting; always plan toward evacuation.
• Documentation of TRENDS (vitals, urine output, mentation, wounds) on the PCC casualty card is a core PCC skill.
• Initiate teleconsult early; in the AFRICOM AOR the 'golden hour' is often a golden day — the hold is the job.

Character Development

Patient. SGT 'Reserve' Park, 26 — resuscitated with initial whole blood after an abdominal GSW with controlled-for-now bleeding, but now 18 hours into a hold with no surgery in sight, showing signs of slow ongoing blood loss (creeping tachycardia, falling urine output, dropping mentation).

Medic. MSG Dolores “Type-O” Park, 39 — senior 18D who knows that DCR in prolonged care is not a one-time event but a sustained balancing act — re-dosing blood, managing the walking blood bank as a renewable resource, and watching for the slow re-bleed.

Environment

Before. A prolonged hold after initial whole-blood resuscitation; the abdominal source is temporarily controlled but not surgically fixed. The team's prescreened donors can give again within limits; calcium and TXA are on hand; teleconsult is available.

During. Park detects the subtle trend of ongoing hemorrhage over hours and must sustain resuscitation — more whole blood from a managed donor pool, repeated calcium, maintaining permissive-hypotension targets, fighting the lethal triad over time — while pushing relentlessly for evacuation to surgery.

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Vital Signs

Physical Examination

Critical Actions

• TREND, DON'T SNAPSHOT: monitor HR, pulse character, mentation, and URINE OUTPUT over time to catch slow re-bleeding.
• SUSTAIN DCR: re-dose whole blood to clinical endpoints; maintain permissive hypotension (SBP ~100; ~100–110 if TBI).
• MANAGE THE WALKING BLOOD BANK as a renewable resource: track donors/units, respect re-donation intervals and donor safety; collect ahead of need.
• CALCIUM with ongoing transfusion (citrate binds calcium — the 'lethal diamond'); give early and repeatedly.
• FIGHT THE LETHAL TRIAD over time: aggressive warming, blood over crystalloid, TXA.
• RE-SURVEY for missed/second hemorrhage source.
• TELECONSULT a surgeon/intensivist; document every unit (donor/time/volume).
• ESCALATE EVACUATION — prolonged DCR is a bridge against a non-compressible bleed, not a cure.

Clinical Pearls

• Prolonged DCR is sustained, adaptive resuscitation over hours/days — trend perfusion (incl. urine output) to catch slow re-bleeding.
• Manage the walking blood bank as a renewable but finite resource: track donors/units, respect re-donation limits and donor safety, collect ahead of need.
• Give CALCIUM early and repeatedly with ongoing transfusion (citrate binds calcium — the 'lethal diamond').
• Resuscitate to clinical endpoints (radial pulse, mentation, urine output ~0.5 mL/kg/hr); permissive hypotension until surgery (higher if TBI).
• A slow re-bleed is a deteriorating trajectory you can't reverse without surgery — escalate evacuation; DCR is a bridge.
• Sustained DCR is austere critical care — the SOF medic may be the ICU for a day or more.

Character Development

Patient. SGT 'Vigil' Okonkwo, 30 — a sedated, intubated casualty (post-surgical-airway, ventilated) being held 36+ hours after blast injury. He's hemodynamically stable, but now at risk from the slow killers of prolonged immobility: pressure injuries, a full bladder, aspiration, eye drying, and unmonitored fluid balance.

Medic. SFC Aimee “Bedside” Okafor, 34 — 18D who knows that once the dramatic injuries are controlled, the casualty in a long hold is killed or maimed by NEGLECT of nursing fundamentals — the unglamorous, checklist-driven care that ICU nurses provide.

Environment

Before. A 36-hour-plus hold of a sedated, ventilated casualty in a 'house' setting. The acute injuries are managed; the threat now is the cumulative harm of prolonged bed-bound critical illness without systematic nursing care. The Nursing Interventions in PCC CPG guides the work.

During. Okafor implements systematic nursing care — monitoring and documenting fluid balance (Foley/urine output), preventing pressure injuries, eye and mouth care, aspiration prevention, repositioning, hygiene, and nutrition planning — treating the 'boring' fundamentals as the life-saving discipline they are.

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Vital Signs

Physical Examination

Critical Actions

• TREAT NURSING FUNDAMENTALS AS LIFE-SAVING — once trauma is controlled, neglect of the basics kills/maims in a long hold.
• FOLEY + HOURLY URINE OUTPUT (target ~0.5 mL/kg/hr) — the best low-tech perfusion/renal monitor; track on a flow sheet.
• REPOSITION q2h; pad/float bony prominences; keep skin clean and DRY — prevent pressure injuries and DVT.
• ASPIRATION PREVENTION: head of bed ~30°, suction, oral care, manage gastric distension.
• EYE CARE: lubricate + tape sedated eyes closed — prevent corneal injury/blindness.
• NUTRITION ('if the gut works, use it' — enteral feeding), hydration, electrolyte and bowel/bladder management over days.
• SECURE and surveil all lines/tubes for infection; mouth care.
• USE PCC nursing checklists/mnemonics (RAVINE/HITMAN) + flow-sheet DOCUMENTATION to make it repeatable.

Clinical Pearls

• After trauma is controlled, the long-hold casualty is killed/maimed by NEGLECTED nursing fundamentals — they are life-saving, not comfort care.
• A Foley + hourly urine output (~0.5 mL/kg/hr) is the best low-tech perfusion/renal monitor in PCC — use a flow sheet.
• Reposition q2h, protect bony prominences, keep skin dry — prevent pressure injuries (which become infected wounds).
• Sedated eyes don't blink — lubricate and tape them closed to prevent corneal ulceration/blindness; elevate head of bed to prevent aspiration.
• Feed the gut if it works; track intake/output, electrolytes, and bowel/bladder over days.
• Use PCC nursing mnemonics/checklists (RAVINE/HITMAN) and documentation — the discipline of the basics, done repeatedly, carries the casualty through.

Character Development

Patient. SGT 'Voice' Bello, 29 — a complex casualty in a prolonged hold (penetrating torso trauma, evolving respiratory difficulty, and a management decision beyond routine protocols) whose care would benefit enormously from a surgeon's or intensivist's input — input the lone medic doesn't have on site.

Medic. SFC Marcus “Relay” Bello, 36 — 18D who knows that in PCC the medic is not alone if they use teleconsultation well — and that the quality of the help received depends entirely on the quality of the information SENT.

Environment

Before. A prolonged hold deep in the AOR with satellite/radio data connectivity to a virtual-health / teleconsultation capability (e.g., the ADVISOR/virtual critical care line). The medic faces decisions — ventilator settings, antibiotic choices, a procedure — above routine scope.

During. Bello organizes and transmits a concise, structured clinical picture to a remote physician, asks focused questions, and integrates the specialist's guidance into the hold — turning a lone medic into a medic backed by a critical-care team over a wire.

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Vital Signs

Physical Examination

Critical Actions

• CALL EARLY: initiate teleconsult when anticipating a prolonged hold or facing a decision beyond routine scope — not when crashing.
• PREPARE A STRUCTURED PICTURE: MIST + SBAR / systems summary — mechanism, injuries, vital + urine-output TRENDS, interventions/response, meds/blood, resources, evacuation timeline.
• ASK FOCUSED, decision-tied questions; transmit photos/data if the channel allows.
• CLOSE THE LOOP: read back the plan, set call-back thresholds, document the guidance and who gave it.
• INTEGRATE guidance while retaining on-scene judgment; re-consult if reality diverges.
• DOCUMENT relentlessly on the PCC casualty card — the backbone of consults, trend recognition, and handoff.
• PLAN FOR LOST CONNECTIVITY — default to CPGs and autonomous judgment; treat telemedicine as an adjunct, not a crutch.

Clinical Pearls

• Initiate teleconsult EARLY — when anticipating a long hold or a decision beyond routine scope, not during a crash.
• The quality of help is bounded by the quality of information sent — use a structured handoff (MIST + SBAR), emphasizing TRENDS.
• Ask focused, decision-tied questions; close the loop with read-backs and call-back thresholds; document who advised what.
• Documentation (PCC casualty card / flow sheet of trends) is the clinical backbone of consults, trend recognition, and handoff.
• Plan for lost connectivity — retain autonomous judgment and CPG-based skills; telemedicine is an adjunct, not a replacement.
• Teleconsultation is a force-multiplier that turns the isolated medic into the hands of a distributed critical-care team.

Character Development

Patient. SGT 'Ember' Park, 28 — 36 hours into a hold after a contaminated extremity wound, now with rising heart rate, rising respiratory rate, a rising then falling temperature, subtle confusion, and decreasing urine output — the early, easily-missed signature of evolving sepsis from a wound infection.

Medic. SFC Owen “Sentinel” Reilly, 35 — 18D who knows that in a long hold the casualty who survived the trauma can be killed by INFECTION, and that by the time blood pressure drops, sepsis is already advanced — you must catch it on the subtle early signs.

Environment

Before. A 36-hour hold of a casualty with a contaminated wound, far from surgery. Source control is incomplete, and infection is evolving into sepsis. The team has tiered antibiotic options and the Sepsis Management in Prolonged Field Care CPG to guide therapy.

During. Reilly recognizes the early, nonspecific signs of sepsis — tachycardia, tachypnea, altered mentation, falling urine output, temperature derangement — BEFORE hypotension, and initiates the sepsis bundle: source control, tiered antibiotics, fluid/perfusion support, and escalated evacuation.

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Vital Signs

Physical Examination

Critical Actions

• DON'T WAIT FOR HYPOTENSION — it's a LATE sign; hunt the early trend: rising HR/RR, new confusion, falling urine output, temp derangement.
• SCREEN with qSOFA (altered mentation, RR ≥22, SBP ≤100 — ≥2 = high risk); the first two appear before the BP criterion.
• SOURCE CONTROL: clean/debride/irrigate the wound, drain abscess, remove infected hardware — antibiotics can't beat an undrained source.
• ANTIBIOTICS EARLY, tiered (PFC CPG): min — moxifloxacin/levofloxacin; better — ertapenem/ceftriaxone 2 g; best — ceftriaxone + vancomycin + metronidazole / carbapenem combo.
• FLUID resuscitation to PERFUSION endpoints (urine output ~0.5 mL/kg/hr, mentation, MAP ~≥65) — avoid OVER-resuscitation.
• MONITOR/TREND on a flow sheet (Foley urine output, mentation, vitals); surveil all sources (wound, line, lung, urine).
• TELECONSULT for antibiotic/source guidance; ESCALATE EVACUATION — septic shock needs higher care/vasopressors.

Clinical Pearls

• Hypotension is a LATE sign of sepsis — by then it's septic shock; act on the early trend (rising HR/RR, new confusion, falling urine output, temp derangement).
• qSOFA (altered mentation, RR ≥22, SBP ≤100; ≥2 = high risk) is a lab-free field screen — the first two criteria precede the BP drop.
• Source control (debride/irrigate/drain/remove) is decisive in wound sepsis — antibiotics can't overcome an undrained source.
• Start antibiotics EARLY, tiered min/better/best per the PFC sepsis CPG (moxi/levo → ertapenem/ceftriaxone → ceftriaxone+vanco+metronidazole).
• Resuscitate to perfusion endpoints (urine output, mentation, MAP ~≥65) — avoid over-resuscitation.
• Teleconsult and escalate evacuation — sepsis is the slow killer of the casualty who survived the trauma.

Character Development

Patient. A partner-force soldier trapped under a collapsed wall/rubble for ~4 hours after a structure failure during an operation, with both legs pinned and crushed. He is alert and talking while entrapped — but releasing the crushed limbs threatens a lethal surge of potassium and toxins into his circulation.

Medic. SFC Talia “Keystone” Mensah, 35 — 18D who knows the cruel paradox of crush injury: the casualty can be stable while trapped and then ARREST the moment the weight comes off, unless you resuscitate and treat hyperkalemia BEFORE and during extrication.

Environment

Before. A prolonged entrapment (~4 hours) under rubble — long enough for crush syndrome to develop in the compressed muscle. The crush-syndrome PFC CPG guides the pre-release resuscitation. Evacuation to dialysis-capable care is far off.

During. Mensah confronts the defining crush-syndrome decision: aggressively resuscitate with fluids and pre-treat hyperkalemia BEFORE releasing the crushed limbs (to dilute and counter the potassium/myoglobin washout), monitor the ECG, and prepare for arrhythmia at the moment of release.

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Vital Signs

Physical Examination