# Clinical Cases: Wilderness Medicine

## Case 1: High Altitude Cerebral Edema

### Patient Presentation
**Demographics:** 36-year-old male investment banker and recreational mountaineer

**Chief Complaint:** "He's confused and can't walk straight — he was fine yesterday at Camp 3."

**History of Present Illness:**
Mr. K.L. is a recreational mountaineer attempting to summit a 6,962 m peak (Aconcagua) in Argentina. He ascended from Base Camp (4,300 m) to Camp 2 (5,500 m) over 3 days, then pushed to Camp 3 (6,000 m) the following day — a 500 m altitude gain in a single day. His climbing partner reports that Mr. K.L. complained of a severe headache and nausea on the evening of arrival at Camp 3 but refused to descend, attributing symptoms to dehydration and fatigue.

The following morning (current presentation), his partner found him confused, unable to zip his jacket, and speaking incoherently. He was unable to perform tandem gait (truncal ataxia — "walking like he was drunk"), had difficulty following simple commands, and appeared disoriented to place and time. He vomited twice. He did not lose consciousness but became progressively more lethargic over 2 hours. His climbing partner initiated descent and radioed for help.

No acetazolamide or dexamethasone prophylaxis was used. The climber had summited a 5,895 m peak (Kilimanjaro) 6 months prior without altitude illness. He had not acclimatized at intermediate elevations prior to this ascent due to time constraints.

**Past Medical History:**
- Migraine headaches (2-3 per year, well-controlled with sumatriptan)
- No prior altitude illness (limited high-altitude experience — one prior climb to 5,895 m)
- No cardiac or pulmonary disease

**Medications:**
- None (did not use chemoprophylaxis)
- Sumatriptan 100 mg PRN (not carried on expedition)

**Social History:**
- Non-smoker, social alcohol
- Regular gym-based fitness routine; completed marathon 4 months ago (sea level)
- Lives in New York City (sea level resident)
- Married, no children
- No prior wilderness medicine training

**Family History:**
- Non-contributory; no known susceptibility to altitude illness

### Physical Examination
- **Vital Signs:** BP 148/92 mmHg, HR 112 bpm, RR 24 (Cheyne-Stokes pattern noted), SpO2 68% on room air at 6,000 m (expected range 72-82%), Temp 35.8°C (tympanic), altitude 6,000 m
- **General:** Appears acutely ill, lethargic, intermittently agitated, does not follow complex commands consistently
- **HEENT:** Pupils 4 mm bilaterally, sluggishly reactive; no papilledema on field fundoscopy (limited examination quality); no facial asymmetry
- **Neurological:**
  - GCS: E3V4M5 = 12 (eye opening to voice, confused speech, localizes pain)
  - Tandem gait: unable to perform — gross truncal ataxia, falls to right side
  - Finger-to-nose: dysmetric bilaterally, right worse than left
  - Motor: moves all extremities spontaneously; no focal weakness on gross testing
  - Reflexes: diffusely brisk (3+); no clonus; Babinski equivocal bilaterally
  - No meningismus
- **Pulmonary:** Bilateral scattered crackles at bases (possible concurrent HAPE); no wheeze
- **Skin:** Mild periorbital edema; facial puffiness noted; no cyanosis despite low SpO2 (acclimatization artifact)
- **Lake Louise Score:** Headache 3 (severe, incapacitating) + GI 2 (moderate nausea/vomiting) + Fatigue 3 (severe) + Dizziness 2 (moderate) + Clinical functional score: altered mental status + ataxia = **HACE criteria met**

### Workup and Results

**Laboratory Studies:**
| Test | Result | Reference Range (sea level) |
|------|--------|-----------------|
| Fingerstick glucose | 78 mg/dL | 70-100 mg/dL |
| SpO2 (pulse oximetry) | 68% | 95-100% (sea level) |
| Core temperature (rectal) | 35.4°C | 36.5-37.5°C |
| GCS | 12/15 | 15/15 |
| Lake Louise AMS Score | 10 (with HACE criteria) | 0-3 normal |

**Imaging/Additional Studies:**
- **Field assessment (limited resources):** No imaging available at altitude
- **Portable ultrasound (carried by expedition medic):** B-line pattern on bilateral lung ultrasound consistent with concurrent high-altitude pulmonary edema; IVC plethoric (3% collapse with respiration — volume status assessment)
- **Post-evacuation MRI brain (performed 48 hours later at sea-level hospital):** T2/FLAIR hyperintensity in the splenium of the corpus callosum and bilateral white matter (centrum semiovale); no hemorrhage; no herniation; findings consistent with vasogenic edema of HACE

### Clinical Image

![Pathophysiology of high altitude cerebral edema](case_01_image.jpg)

*Illustration depicting the pathophysiology of high altitude cerebral edema (HACE), showing hypoxia-driven disruption of the blood-brain barrier, vasogenic edema, and cerebral swelling with characteristic involvement of the corpus callosum. Source: Educational illustration.*

### Diagnosis
**High Altitude Cerebral Edema (HACE) with Concurrent High Altitude Pulmonary Edema (HAPE)**

**Key Diagnostic Criteria:**
- Altitude >2,500 m with recent ascent history
- Altered mental status (confusion, disorientation, GCS 12) in a person with symptoms of acute mountain sickness
- Truncal ataxia (unable to perform tandem gait) — the hallmark clinical finding of HACE
- Lake Louise AMS score ≥5 with clinical criteria for HACE (altered consciousness or ataxia)
- Concurrent HAPE (crackles, B-lines on ultrasound) — HACE and HAPE frequently coexist
- Rapid ascent rate (500 m/day above 5,500 m) without acclimatization or chemoprophylaxis
- Post-evacuation MRI confirming vasogenic edema with classic splenium of corpus callosum involvement

### Treatment Plan
1. **Immediate descent (the definitive treatment):**
   - Descend minimum 1,000 m (to Camp 1 at 5,000 m or lower) as rapidly as safely possible
   - If descent is impossible (weather, terrain): portable hyperbaric chamber (Gamow bag or Certec bag) at 2 psi for 2-4 hours
2. **Supplemental oxygen:**
   - High-flow O2 via mask: 4-6 L/min (target SpO2 >90%)
   - Continue during descent and transport
3. **Dexamethasone:**
   - 8 mg IM/IV immediately (loading dose), then 4 mg IM/IV/PO every 6 hours
   - Continue for 24-48 hours after descent until symptoms resolve; taper over 2-3 days
4. **Concurrent HAPE treatment:**
   - Nifedipine 30 mg extended-release PO (reduces pulmonary artery pressure)
   - Supplemental oxygen (as above — treats both HACE and HAPE)
   - Descent is the primary treatment for both conditions
5. **Supportive care:**
   - Rewarming: insulate from ground, warm fluids, sleeping bag
   - Oral or IV fluids if able to swallow safely (monitor airway in altered patient)
   - Monitor GCS every 30 minutes during descent
   - NPO if GCS <13 or actively vomiting (aspiration risk)
6. **Evacuation:** Helicopter evacuation to the nearest medical facility once weather permits; arrange transfer to hospital with neurology and critical care capability
7. **Post-event:**
   - Observation minimum 48 hours at low altitude
   - MRI brain to document extent of edema and rule out alternative diagnoses
   - Neurocognitive assessment after resolution
   - Counseling regarding future altitude exposure: high recurrence risk; if future ascent planned, slow accent profile with acetazolamide prophylaxis mandatory; consider dexamethasone for ascent above 5,000 m

### Key Learning Points
- HACE is a life-threatening medical emergency with mortality approaching 60-80% if untreated; it represents the end-stage of acute mountain sickness (AMS) and results from vasogenic edema due to hypoxia-induced disruption of the blood-brain barrier
- Truncal ataxia (inability to perform tandem gait) is the most reliable early clinical sign of HACE and should trigger immediate descent; waiting for altered consciousness risks rapid progression to coma and death
- Descent is the definitive treatment for HACE — a descent of 500-1,000 m typically produces dramatic improvement; dexamethasone buys time but does not replace descent
- The "golden rules" of altitude medicine: (1) ascend gradually (no more than 300-500 m sleeping altitude gain per day above 3,000 m), (2) any symptom at altitude is altitude illness until proven otherwise, (3) never ascend with symptoms of AMS, (4) descend if symptoms worsen
- HACE and HAPE frequently coexist (40-50% overlap) and share the underlying pathophysiology of maladaptive response to hypobaric hypoxia; treatment of one should include assessment for the other

---

## Case 2: Lightning Strike Injury

### Patient Presentation
**Demographics:** 24-year-old female park ranger

**Chief Complaint:** "She was struck by lightning on the trail — she was unconscious for a couple of minutes and now she can't hear."

**History of Present Illness:**
Ranger M.J. was leading a group of 8 hikers along an exposed alpine ridge trail at 3,200 m elevation when a sudden thunderstorm developed. While attempting to guide the group below treeline, she was struck by lightning via a side flash/splash mechanism — lightning struck a nearby metal trail sign and arced to the patient, who was approximately 2 meters away. Witnesses report she was thrown approximately 1.5 meters, was motionless and pulseless for an estimated 60-90 seconds, then began gasping and moving spontaneously.

Upon regaining consciousness approximately 2 minutes after the strike, she was confused and disoriented, complained of severe bilateral hearing loss with tinnitus, and reported burning pain in her left arm and left leg. She had no memory of the event (retrograde amnesia). One of the hikers, a nurse, performed a primary survey: airway patent, breathing spontaneously, pulse present (irregular), GCS improved to 14 within 10 minutes.

On further assessment by a wilderness EMT who arrived within 45 minutes, she was noted to have Lichtenberg figures (ferning pattern) across her left shoulder and arm, first-degree burns at the left hand (metal watch), and bilateral tympanic membrane ruptures. She was unable to hear conversational speech. She complained of bilateral lower extremity weakness and paresthesias.

**Past Medical History:**
- No significant medical history
- No prior lightning exposure or electrical injury
- Up to date on tetanus immunization

**Medications:**
- Oral contraceptive pill
- Multivitamin

**Social History:**
- Non-smoker, occasional alcohol
- Avid outdoor enthusiast (hiking, climbing, skiing)
- 3 years as a National Park Service ranger
- Wilderness First Responder certified

**Family History:**
- Non-contributory

### Physical Examination
- **Vital Signs:** BP 102/68 mmHg, HR 108 bpm (irregular), RR 18, SpO2 97% on room air, Temp 36.2°C (mild hypothermia from rain and exposure), GCS 14 (E4V4M6)
- **General:** Alert, anxious, communicating via hand signals and lip reading due to hearing loss
- **HEENT:**
  - Eyes: bilateral fixed dilated pupils (6 mm bilateral — autonomic dysfunction, not necessarily indicative of brain injury in lightning); corneas clear; no hyphema
  - Ears: bilateral tympanic membrane perforation (right: central perforation ~40%; left: marginal perforation ~60%); hemorrhagic otorrhea bilaterally; unable to hear conversational speech bilaterally (estimated >60 dB hearing loss); no hemotympanum beyond TM rupture
  - Oropharynx: clear, no burns
- **Skin/Burns:**
  - Lichtenberg figures (pathognomonic ferning/fern-like pattern): extending from left shoulder across left deltoid to left forearm — superficial, non-blanching, arborescent erythema
  - First-degree burn with central blister at left wrist (beneath metal watchband — contact point)
  - Linear burn along left lateral leg (flashover path)
  - Total body surface area (TBSA) burned: <2% (superficial)
- **Cardiovascular:** Irregular rhythm; no murmurs; distal pulses present but diminished in left upper extremity; capillary refill 3 seconds left hand
- **Neurological:**
  - Mental status: oriented to person and place, not time; retrograde amnesia for event; anterograde memory impaired (cannot recall 3 objects at 5 minutes)
  - Motor: lower extremity weakness bilateral — hip flexion 3/5, knee extension 4/5, ankle dorsiflexion 4/5 (keraunoparalysis — lightning-specific transient paralysis)
  - Sensory: diminished sensation bilateral lower extremities below knees; paresthesias bilateral feet
  - Reflexes: absent bilateral lower extremities (areflexia — consistent with keraunoparalysis)
  - Upper extremity exam: left grip strength reduced 3/5; right 5/5
- **Musculoskeletal:** No obvious fractures on palpation; no spinal tenderness; no compartment syndrome signs

### Workup and Results

**Laboratory Studies:**
| Test | Result | Reference Range |
|------|--------|-----------------|
| Troponin I (field POC) | 0.18 ng/mL | <0.04 ng/mL |
| CPK (hospital) | 2,840 U/L | 26-192 U/L |
| Myoglobin | 580 ng/mL | 28-72 ng/mL |
| Creatinine | 1.3 mg/dL | 0.6-1.1 mg/dL |
| Potassium | 5.4 mEq/L | 3.5-5.0 mEq/L |
| Lactate | 4.2 mmol/L | 0.5-2.0 mmol/L |
| Urinalysis | Dark brown, myoglobin positive | - |
| BhCG | Negative | - |

**Imaging/Additional Studies:**
- **Field ECG (portable monitor):** Sinus tachycardia with frequent PVCs; QTc prolonged at 510 ms; no ST elevation or depression; no evidence of acute MI pattern
- **Hospital ECG (4 hours post-strike):** Sinus rhythm, 96 bpm; PVCs decreased; QTc 480 ms; diffuse T-wave flattening
- **CT head (hospital):** No intracranial hemorrhage, no fracture, no edema
- **CT cervical/thoracic/lumbar spine:** No fractures
- **Chest X-ray:** No pneumothorax, no pulmonary contusion
- **Echocardiogram (hospital):** Normal LV function, EF 55%; no regional wall motion abnormalities; no pericardial effusion; mild tricuspid regurgitation
- **Audiometry (day 3):** Bilateral mixed hearing loss — conductive component from TM perforation + sensorineural component (likely cochlear blast injury); right ear: 55 dB PTA; left ear: 65 dB PTA

### Clinical Image

![Lightning strike injury mechanisms and clinical findings](case_02_image.jpg)

*Illustration depicting the mechanisms of lightning injury (direct strike, side flash, ground current, contact, upward streamer), pathognomonic Lichtenberg figures, and the concept of keraunoparalysis with autonomic dysfunction. Source: Educational illustration.*

### Diagnosis
**Lightning Strike Injury (Side Flash Mechanism) with Cardiac Contusion, Keraunoparalysis, Bilateral Tympanic Membrane Rupture, Rhabdomyolysis, and Traumatic Brain Injury (Mild)**

**Key Diagnostic Criteria:**
- Witnessed lightning strike with transient cardiopulmonary arrest and spontaneous ROSC
- Lichtenberg figures (pathognomonic for lightning injury — not seen in other electrical injuries)
- Keraunoparalysis: bilateral lower extremity paralysis with areflexia and autonomic dysfunction (fixed dilated pupils, vasospasm) — a transient phenomenon unique to lightning injury
- Bilateral TM perforation (blast effect from thunder/pressure wave — occurs in >50% of lightning strike survivors)
- Elevated troponin and CPK indicating cardiac and skeletal muscle injury
- Myoglobinuria indicating rhabdomyolysis
- Prolonged QTc (risk of torsades de pointes)

### Treatment Plan
1. **Field management (immediate):**
   - C-spine stabilization (fall/throw mechanism)
   - Continuous cardiac monitoring (portable); have AED immediately available
   - IV access: normal saline bolus 1L for rhabdomyolysis prevention
   - Protect from hypothermia (remove wet clothing, insulate)
   - Reassess neurological function every 15 minutes (keraunoparalysis should begin improving within 1-4 hours)
   - Do NOT be deceived by bilateral fixed dilated pupils — this is autonomic dysfunction, not brain death, in lightning victims
2. **Hospital management:**
   - **Cardiac:** Continuous telemetry for minimum 24 hours (risk of delayed arrhythmias with prolonged QTc); serial troponins Q6H x 24 hours; repeat echocardiogram at 48 hours; electrolyte correction (potassium trending high — avoid further supplementation)
   - **Rhabdomyolysis:** Aggressive IV fluid resuscitation (NS at 200-300 mL/hr targeting UOP 200-300 mL/hr); consider sodium bicarbonate drip to alkalinize urine (target pH >6.5); monitor CPK, myoglobin, creatinine, potassium Q6H until trending down
   - **Renal protection:** Maintain high urine output; avoid nephrotoxins; consider mannitol if urine output drops despite aggressive hydration
3. **Otologic management:**
   - ENT consultation for bilateral TM perforations
   - Keep ears dry; no ear drops initially
   - Serial audiometry at 2 weeks, 6 weeks, 3 months
   - Most TM perforations from lightning heal spontaneously (85%); tympanoplasty if no healing by 3 months
   - Sensorineural component may be permanent
4. **Neurological follow-up:**
   - Serial neurological exams; keraunoparalysis expected to resolve within 24 hours (if not, investigate for spinal cord injury)
   - Neuropsychological testing at 2 weeks and 3 months (lightning survivors have high incidence of persistent cognitive deficits: memory impairment, attention deficits, personality changes)
   - MRI brain if cognitive symptoms persist
5. **Burns:** Wound care for superficial burns; Lichtenberg figures are not true burns and require no specific treatment (they resolve within 24-48 hours)
6. **Psychological support:** Referral for PTSD screening and treatment (high incidence in lightning survivors); Lightning Strike and Electric Shock Survivors International (LSESSI) peer support referral

### Key Learning Points
- Lightning injury is unique among electrical injuries: the current flow is extremely brief (1-5 milliseconds) and flows primarily over the body surface (flashover effect), resulting in relatively low internal tissue damage compared to high-voltage electrical injuries; however, cardiac arrest is the primary cause of death
- The reverse triage principle applies in mass lightning casualty events: treat the apparently dead first (those in cardiac arrest), as they have the best chance of survival with immediate CPR; those who are conscious are likely to survive without immediate intervention
- Keraunoparalysis (lightning-specific transient paralysis with autonomic dysfunction) is self-limiting and resolves within hours; bilateral fixed dilated pupils in lightning victims do NOT indicate brain death and should NOT be used as criteria to withhold resuscitation
- Tympanic membrane rupture is the most common physical finding in lightning strike survivors (>50%) and serves as a marker of significant exposure; bilateral perforation suggests close proximity to the strike point
- Lightning injury survivors frequently develop delayed neuropsychiatric sequelae including PTSD, depression, chronic pain, cognitive impairment, and personality changes; long-term follow-up and psychological support are essential

---

## Case 3: Marine Envenomation (Box Jellyfish)

### Patient Presentation
**Demographics:** 19-year-old male university student on spring break

**Chief Complaint:** "Something stung me in the water — my chest is tight and I can't breathe."

**History of Present Illness:**
Mr. A.T. was swimming at a beach in northern Queensland, Australia at approximately 1400 hours when he felt immediate, excruciating pain across his right arm, right lateral chest, and right abdomen. He screamed and ran out of the water. Bystanders noted long, linear, erythematous, tentacle-pattern marks across the affected areas. Within 2-3 minutes, he developed severe chest tightness, dyspnea, nausea, and profuse diaphoresis. He became pale and felt like he was "going to die."

Lifeguards responded within 4 minutes and identified the injury as a probable major box jellyfish (Chironex fleckeri) sting based on the tentacle pattern, season (November — wet season/stinger season), and geographic location. They immediately doused the sting areas with household vinegar for 30 seconds, removed adherent tentacles using gloved hands, and called for ambulance paramedics. An EpiPen was administered by one lifeguard who suspected anaphylaxis, though the presentation was subsequently assessed as direct envenomation rather than allergic reaction.

En route to hospital (25-minute transport), the patient developed progressive hypotension, became obtunded, and developed a broad-complex tachycardia on the cardiac monitor. IV access was established and a 500 mL NS bolus administered. Box jellyfish antivenom was not available pre-hospital.

**Past Medical History:**
- No significant medical history
- No prior jellyfish stings
- No known allergies

**Medications:**
- None

**Social History:**
- University student studying marine biology (ironic context)
- Non-smoker
- Social alcohol (2-3 beers consumed earlier that day)
- Visiting from Melbourne (not familiar with local stinger dangers)
- No stinger suit worn despite posted warnings at beach

**Family History:**
- Non-contributory

### Physical Examination
- **Vital Signs (arrival to ED):** BP 78/52 mmHg, HR 138 bpm (irregular, wide-complex), RR 28, SpO2 88% on 15L NRB mask, Temp 36.0°C, GCS 10 (E2V3M5)
- **General:** Obtunded, diaphoretic, marked pallor, in severe distress
- **Skin/Envenomation:**
  - Linear, whip-like, erythematous-to-violaceous "frosted ladder" pattern tentacle marks across right forearm extending to right lateral chest wall and right upper abdomen
  - Estimated sting surface area: ~20% of one arm plus ~10% of trunk = significant contact area (>4-5 meters of tentacle contact estimated)
  - Cross-hatched "frosted" appearance typical of C. fleckeri nematocyst discharge pattern
  - Surrounding skin edematous with early vesiculation
  - No urticaria or angioedema (not anaphylaxis)
- **Cardiovascular:** Tachycardic, irregular; wide-complex rhythm on monitor (ventricular tachycardia); weak peripheral pulses; mottled extremities; capillary refill 5 seconds
- **Pulmonary:** Tachypneic; bilateral diffuse crackles; accessory muscle use; no wheeze (argues against anaphylaxis)
- **Neurological:** GCS 10; pupils 5 mm bilateral, reactive; no focal deficits; generalized agitation alternating with obtundation
- **Abdomen:** Guarding over right upper quadrant and flank at sting site; tender along tentacle tracks

### Workup and Results

**Laboratory Studies:**
| Test | Result | Reference Range |
|------|--------|-----------------|
| Troponin I | 2.4 ng/mL | <0.04 ng/mL |
| CPK | 1,850 U/L | 26-192 U/L |
| CK-MB | 48 ng/mL | <5 ng/mL |
| Potassium | 6.8 mEq/L | 3.5-5.0 mEq/L |
| Calcium (ionized) | 0.92 mmol/L | 1.12-1.32 mmol/L |
| Magnesium | 1.4 mg/dL | 1.7-2.2 mg/dL |
| Lactate | 8.2 mmol/L | 0.5-2.0 mmol/L |
| pH (ABG) | 7.18 | 7.35-7.45 |
| pCO2 | 32 mmHg | 35-45 mmHg |
| pO2 | 62 mmHg (on 15L) | 80-100 mmHg |
| Bicarbonate | 14 mEq/L | 22-26 mEq/L |
| INR | 1.6 | 0.8-1.2 |
| Fibrinogen | 148 mg/dL | 200-400 mg/dL |

**Imaging/Additional Studies:**
- **ECG:** Wide-complex tachycardia (ventricular tachycardia) at 138 bpm; ST elevation in V1-V3 with reciprocal ST depression in lateral leads; peaked T-waves consistent with hyperkalemia
- **Chest X-ray:** Bilateral diffuse pulmonary edema (non-cardiogenic — venom-induced capillary leak)
- **Point-of-care echocardiogram:** Severely reduced LV function, estimated EF 25-30%; global hypokinesis; no pericardial effusion; IVC dilated with minimal respiratory variation
- **Repeat ECG (post-treatment, 2 hours):** Sinus tachycardia 110 bpm, narrow complex; ST changes resolving; QTc 490 ms

### Clinical Image

![Box jellyfish envenomation and Chironex fleckeri venom mechanism](case_03_image.jpg)

*Illustration showing the box jellyfish (Chironex fleckeri) tentacle nematocyst discharge mechanism, characteristic "frosted ladder" sting pattern on skin, and the cardiotoxic venom pathways leading to myocardial depression and cardiovascular collapse. Source: Educational illustration.*

### Diagnosis
**Severe Chironex fleckeri (Box Jellyfish) Envenomation with Cardiovascular Collapse, Venom-Induced Cardiomyopathy, Hyperkalemia, and Non-Cardiogenic Pulmonary Edema**

**Key Diagnostic Criteria:**
- Geographic and seasonal context: northern Queensland, Australia during wet/stinger season (October-May)
- Characteristic C. fleckeri sting pattern: linear "frosted ladder" tentacle marks with cross-hatched nematocyst pattern
- Extensive sting surface area (estimated >4-5 m tentacle contact — major envenomation)
- Cardiovascular collapse with cardiogenic shock (EF 25-30%, wide-complex tachycardia)
- Massively elevated troponin and CK-MB indicating severe myocardial injury
- Hyperkalemia (6.8 mEq/L) — venom-induced cell lysis and direct cardiac membrane toxicity
- Metabolic acidosis with elevated lactate — shock physiology

### Treatment Plan
1. **Immediate resuscitation (ED):**
   - **Airway:** RSI and intubation (GCS 10, pulmonary edema, impending respiratory failure); ketamine preferred induction agent (hemodynamic stability)
   - **Breathing:** Mechanical ventilation with PEEP 10 cmH2O for pulmonary edema
   - **Circulation:** IV crystalloid boluses (cautious in cardiogenic shock); vasopressor initiation: norepinephrine 0.1 mcg/kg/min titrated to MAP >65 mmHg
2. **Box jellyfish antivenom (CSL Chironex fleckeri antivenom):**
   - 3 vials (60,000 units) IV diluted in 100 mL NS, infused over 15 minutes
   - Repeat with additional 3 vials if no clinical improvement at 30 minutes (up to 6 vials total for severe envenomation)
   - Monitor for anaphylaxis to antivenom (have epinephrine ready)
3. **Hyperkalemia management (emergent):**
   - Calcium gluconate 10% — 30 mL IV over 5 minutes (cardiac membrane stabilization)
   - Insulin 10 units IV + dextrose 50% 50 mL (intracellular potassium shift)
   - Sodium bicarbonate 50 mEq IV (treats acidosis and shifts potassium)
   - Continuous cardiac monitoring; repeat potassium at 30 and 60 minutes
4. **Cardiovascular support:**
   - Dobutamine 5-10 mcg/kg/min for inotropic support (EF 25-30%)
   - Magnesium sulfate 2 g IV (hypomagnesemia correction + antiarrhythmic)
   - Amiodarone 150 mg IV if VT recurs (avoid in torsades; use Mg first)
   - Serial echocardiography every 6-12 hours
5. **Local wound management:**
   - Vinegar (4-6% acetic acid) was appropriately applied in field (inactivates undischarged nematocysts — specific to C. fleckeri)
   - Do NOT apply fresh water, ice, or pressure bandage (can trigger nematocyst discharge)
   - Gentle removal of remaining tentacle fragments with forceps
   - Wound care: clean with saline, apply non-adherent dressings; monitor for necrosis
6. **ICU management:**
   - Continuous invasive hemodynamic monitoring (arterial line, central venous catheter)
   - Correct metabolic acidosis, hypocalcemia, hypomagnesemia
   - DIC monitoring: serial coagulation studies, fibrinogen, platelet count
   - Rhabdomyolysis protocol: aggressive IV fluids, maintain UOP >1 mL/kg/hr
   - Pain management: IV morphine titrated (severe pain from sting sites)
7. **Follow-up:** ICU stay anticipated 3-7 days; echocardiography before discharge to document LV recovery (venom-induced cardiomyopathy is usually reversible); dermatology follow-up for sting site scarring; psychological support for acute traumatic event

### Key Learning Points
- Chironex fleckeri (Australian box jellyfish) is the most venomous marine animal and one of the most venomous creatures on Earth; deaths can occur within 2-5 minutes of severe envenomation, primarily from cardiovascular collapse due to direct cardiotoxic venom effects
- The venom contains CfTX-1 and CfTX-2 — potent pore-forming toxins that create holes in cell membranes, leading to massive ion flux (potassium release, calcium influx), myocardial depression, and cardiovascular collapse; hyperkalemia is a major mechanism of death
- Vinegar (4-6% acetic acid) is the recommended first aid for C. fleckeri stings as it inactivates undischarged nematocysts; this is specific to box jellyfish — for other jellyfish species (e.g., Physalia/bluebottle), hot water immersion (45°C for 20 minutes) is preferred
- CSL Box Jellyfish Antivenom should be administered IV for severe envenomation; it neutralizes circulating venom but cannot reverse tissue damage already sustained; early administration is critical
- Prevention is paramount in endemic areas: stinger nets at beaches, full-body lycra stinger suits, awareness of seasonal risk (October-May in northern Australia), and heeding beach warning signs and closures