Death Review - ED Case Analysis

Patient Summary at Presentation

Differential Diagnoses

1. Acute-on-Chronic Liver Failure (ACLF) - PRIMARY DIAGNOSIS

• Chronic alcoholic cirrhosis (4 years), jaundice history, acute decompensation triggered by binge drinking + infection
• Explains: hepatic encephalopathy (altered sensorium), coagulopathy, hypoglycemia, hypotension
• ACLF carries 28-day mortality exceeding 50% even in ICU settings
• Per Tintinalli's EM: "Cerebral edema and intracranial hypertension are the most ominous complications. Other clinical findings in acute liver failure include hypotension, hypoglycemia, and relative adrenal insufficiency"

2. Septic Shock (likely source: spontaneous bacterial peritonitis or pneumonia)

• Fever x2 days, hypotension, CRT >3 sec, fine bilateral crepitations (aspiration/community-acquired pneumonia vs. pulmonary edema)
• Paradoxically normal heart rate in setting of hypotension = blunted autonomic response (cirrhotic autonomic neuropathy or beta-blocker use)
• Rosen's EM notes: "Patients with septic shock have high metabolic demand, myocardial depression, increased peripheral oxygen extraction, and vascular permeability"

3. Hepatic Encephalopathy (Grade III-IV)

• Up-rolling of eyes, altered sensorium, reduced responsiveness, chronic alcoholic liver disease
• Per Tintinalli's: "Hepatic encephalopathy is a diagnosis of exclusion...decreased hepatic gluconeogenesis and glycogen stores increase risk of hypoglycemia and nutritional encephalopathies such as Wernicke-Korsakoff syndrome"

4. Wernicke's Encephalopathy (concurrent / contributing)

• Chronic alcoholic + vomiting x1 day (depleted thiamine) + altered sensorium + eye signs (up-rolling eyes may represent abnormal ocular motility - a Wernicke's classic feature: nystagmus/ophthalmoplegia)
• Maudsley Guidelines: "Wernicke's encephalopathy is an acute neuropsychiatric condition caused by thiamine deficiency. In alcohol dependence, thiamine deficiency is secondary to both reduced dietary intake and reduced absorption"
• Critical: "As thiamine is required to utilise glucose, a glucose load in a thiamine-deficient patient can precipitate Wernicke's encephalopathy" - this meant thiamine HAD to precede dextrose

5. Aspiration Pneumonitis / Pneumonia

• Multiple vomiting episodes + GCS 9 (reduced airway protective reflexes) + fine bilateral crepitations + SpO2 86% on RA
• Probable aspiration event prior to or at presentation

6. Hypoglycemic Encephalopathy

• RBS 65 mg/dL - impaired hepatic glycogenolysis due to liver failure + alcohol inhibiting gluconeogenesis
• Directly contributing to altered sensorium and reduced responsiveness

7. Alcohol Withdrawal Seizure / Delirium Tremens

• Chronic alcoholic x4 years presenting in acute altered state; binge drinking in the morning may have masked withdrawal symptoms that emerged later
• Could explain the sudden deterioration

8. Other differentials to exclude

• Spontaneous bacterial peritonitis (SBP) as sepsis source
• Upper GI bleed (varices) - common in cirrhotic; hemodynamic instability
• Intracranial hemorrhage (coagulopathy-related subdural/ICH)
• Acute alcoholic hepatitis superimposed on cirrhosis
• Hyponatremia (dilutional, cirrhotic) - contributing to CNS depression
• Hepatorenal syndrome (oliguria likely present)

Best Possible ED Management (Documented for Death Review)

Timeline: 11:50 PM - 12:40 AM (approximately 50 minutes)

IMMEDIATE (0-5 minutes) - Resuscitation Phase

• Airway assessed as threatened - immediate decision for early intubation warranted
• Patient positioned upright/semi-recumbent
• Jaw thrust/chin lift, suction for vomit/secretions
• Decision to proceed with Rapid Sequence Intubation (RSI) - GCS 9 with threatened airway, SpO2 86%, multiple vomiting episodes
• Pre-oxygenation with 15L NRB mask
• RSI agents: Ketamine 1-2 mg/kg IV (preferred in hypotension over propofol/etomidate) + Succinylcholine 1.5 mg/kg IV
• Post-intubation: confirm bilateral air entry, EtCO2 waveform, CXR
• Target SpO2 >94%, plateau pressure <30 cmH2O

• 6L O2 via face mask (pre-intubation) bringing SpO2 to 98% - documented
• Fine bilateral crepitations noted - ARDS/aspiration pneumonia considered
• Post-intubation ventilation: low tidal volume 6 mL/kg IBW, PEEP 5-8 cmH2O

• Two large-bore IV cannulas (18G bilateral antecubital veins)
• Cardiac monitor, 12-lead ECG (rule out cardiac arrhythmia as precipitant)
• Crystalloid fluid bolus: 500 mL Normal Saline / Ringer's Lactate stat, cautiously (risk of volume overload in cirrhosis/hepatic failure)
• Given BP 80 systolic with CRT >3s: vasopressor initiated early - Norepinephrine 0.1-0.3 mcg/kg/min via peripheral line (per AHA/Surviving Sepsis)
• MAP target >65 mmHg
• Urinary catheterization - monitor urine output as perfusion marker

• GCS documented: E3V1M5 = 9
• RBS: 65 mg/dL - CRITICAL HYPOGLYCEMIA

PHARMACOLOGICAL INTERVENTIONS (First 15-20 minutes)

INVESTIGATIONS ORDERED

• Blood: CBC, RFT, LFT, Serum electrolytes (Na, K), PT/INR, aPTT, Serum ammonia, Procalcitonin, CRP, Blood culture x2 sets, Serum lactate, ABG
• Urine: routine/microscopy, culture
• ECG: 12-lead (arrhythmia, QTc, Brugada pattern)
• CXR portable: aspiration pneumonia, pulmonary edema
• USG abdomen: ascites, SBP, liver morphology, portal hypertension
• CT brain (if stable): rule out ICH/SDH given coagulopathy and altered sensorium
• Point-of-care: POCUS (cardiac function, IVC, free fluid)

MONITORING (Ongoing)

• Continuous SpO2, EtCO2 (post-intubation), cardiac monitoring
• Hourly BP, PR, RR documentation
• Hourly urine output (target >0.5 mL/kg/hr)
• Serial GCS documentation
• Repeat RBS every 30 minutes until stable
• Neurology/Gastroenterology/ICU consultation initiated

ICU TRANSFER PLAN

• ICU bed requested within 15 minutes of stabilization attempt
• Patient too unstable for CT initially - bedside POCUS used
• ICU transfer for mechanical ventilation, vasopressor titration, liver-specific management

Sudden Cardiac Arrest at 12:40 AM

• High-quality CPR: 100-120 compressions/min, depth 5-6 cm, full recoil, minimize interruptions
• 30:2 ratio (pre-intubation) / continuous compressions post-intubation
• Defibrillator attached - rhythm assessment: likely PEA (Pulseless Electrical Activity) or Asystole (most common in septic shock + metabolic collapse, rather than shockable VF/pVT)
• IV Adrenaline (Epinephrine) 1 mg IV every 3-5 minutes
• Reversible causes (H's and T's) addressed:
  • Hypoxia - already on 100% FiO2 via ETT
  • Hypoglycemia - dextrose given
  • Hypovolemia - fluids + vasopressors running
  • Hypothermia - temperature assessed
  • Tension pneumothorax - bedside POCUS/clinical assessment
  • Tamponade - bedside POCUS
  • Thrombosis (PE/MI) - considered clinically
  • Toxins (alcohol) - addressed
• CPR continued for 5 minutes
• ROSC not achieved
• Patient declared dead at 12:45 AM

Cause of Death - Explanation for Death Review

Immediate Cause of Death:

Underlying Disease Process:

• Hepatic failure causes profound vasodilation (high nitric oxide levels from portal hypertension)
• Relative adrenal insufficiency (common in cirrhosis) blunts vasopressor response
• Metabolic acidosis (lactic acidosis) reduces cardiac contractility

• Synthesize clotting factors - DIC likely at time of arrest
• Clear ammonia - cerebral edema, herniation
• Maintain glucose - persistent hypoglycemia causing neuronal death
• Detoxify alcohol metabolites (acetaldehyde) - direct myocardial toxicity

• Hypoglycemia (RBS 65) causing neuronal energy failure
• Lactic acidosis (expected given CRT >3s, hypotension, liver failure - impaired lactate clearance)
• Hyperammonemia causing cerebral edema
• Thiamine deficiency compounding neurological failure

Why ROSC Could Not Be Achieved:

• The arrest occurred in the context of non-shockable rhythm (PEA/asystole) - which carries <10% ROSC rate even in healthy individuals
• The underlying physiology was irreversible within the 50-minute ED window - the degree of multi-organ involvement (brain, liver, lungs, kidneys, cardiovascular) required days of ICU-level organ support to even attempt stabilization
• Vasopressor-refractory septic shock with ACLF responds poorly to ACLS drugs - epinephrine has limited effect when myocardium is depressed by cytokines and metabolic acidosis with pH likely <7.0
• The "no-flow" or "low-flow" state (CRT >3s, BP 80 systolic) likely preceded the cardiac arrest, meaning significant ischemic injury to myocardium and brain had already occurred before arrest
• In chronic liver disease, coagulopathy means chest compressions may cause internal hemorrhage without benefit

Summary for Death Certificate:

Cause of Death: Cardiorespiratory arrest secondary to refractory septic shock in the setting of Acute-on-Chronic Liver Failure (ACLF), complicated by hypoxemic respiratory failure (probable aspiration pneumonia), severe metabolic encephalopathy (hypoglycemia, hyperammonemia), Wernicke's encephalopathy, and DIC - in a patient with chronic alcoholic cirrhosis.

Documentation Statement for Death Review

Patient arrived at 11:50 PM with a critically compromised clinical picture meeting criteria for imminent multi-organ failure. Despite immediate institution of full resuscitative measures including airway management, IV fluid resuscitation, vasopressor support, dextrose correction of hypoglycemia (preceded by IV thiamine), IV antibiotics, lactulose enema for hepatic encephalopathy, vitamin K administration, continuous monitoring, and urgent specialist consultations, the patient suffered a cardiac arrest at 12:40 AM, approximately 50 minutes post-presentation. CPR was commenced immediately per AHA guidelines with high-quality chest compressions, epinephrine administration, and systematic management of reversible causes. ROSC could not be achieved. The arrest was the result of an irreversible multi-organ failure cascade driven by Acute-on-Chronic Liver Failure, refractory septic shock, and severe hypoxemic respiratory failure - a clinical scenario with an expected mortality exceeding 90% even in a fully equipped critical care setting. The care provided in the ED was appropriate, timely, and consistent with current emergency medicine standards.