Hypotension

Brief H&P:

A 50 year-old male with a history of colonic mucinous adenocarcinoma on chemotherapy presented with a chief complaint of “vomiting”. He was unwilling to provide further history, repeating that he had vomited blood prior to presentation. His initial vital signs were notable for tachycardia. Physical examination showed some dried vomitus, brown in color, at the nares and lips; left upper quadrant abdominal tenderness to palpation; and guaiac-positive stool. Point-of-care hemoglobin was 3g/dL below the most recent measure two months prior. As his evaluation progressed, he developed hypotension and was transfused two units of uncrossmatched blood with adequate blood pressure response – he was started empirically on broad-spectrum antibiotics for an intra-abdominal source. Notable laboratory findings included a normal hemoglobin/hematocrit, acute kidney injury, and elevated anion gap metabolic acidosis presumably attributable to serum lactate of 10.7mmol/L. Computed tomography of the abdomen and pelvis demonstrated pneumoperitoneum with complex ascites concerning for bowel perforation. The patient deteriorated, was intubated, started on vasopressors and admitted to the surgical intensive care unit. The initial operative report noted extensive adhesions and perforated small bowel with feculent peritonitis. He has since undergone multiple further abdominal surgeries and remains critically ill.

Imaging

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CT Abdomen/Pelvis

Free air is seen diffusely in the non-dependent portions of the abdomen: in the anterior abdomen and pelvis, inferior to the diaphragm, and in the perisplenic region. There is complex free fluid in the abdomen.

Algorithm for the Evaluation of Hypotension1

This process for the evaluation of hypotension in the emergency department was developed by Dr. Ravi Morchi. In the case above, a systematic approach to the evaluation of hypotension using ultrasonography and appropriately detailed physical examination may have expedited the patient’s care. The expertly-designed algorithm traverses the cardiovascular system, halting at evaluable checkpoints that may contribute to hypotension.

  1. The process begins with the cardiac conduction system to identify malignant dysrhythmias (bradycardia, or non-sinus tachycardia >170bpm), which, in unstable patients are managed with electricity.
  2. The next step assesses intravascular volume with physical examination or bedside ultrasonography of the inferior vena cava. Decreased right atrial pressure (whether due to hypovolemia, hemorrhage, or a distributive process) is evidenced by a small and collapsible IVC. If hemorrhage is suspected, further ultrasonography with FAST and evaluation of the abdominal aorta may identify intra- or retroperitoneal bleeding.
  3. If a normal or elevated right atrial pressure is identified, evaluate for dissociation between the RAP and left ventricular end-diastolic volume. This is typically caused by a pre- or intra-pulmonary obstructive process such as tension pneumothorax, cardiac tamponade, massive pulmonary embolism, pulmonary hypertension, or elevated intra-thoracic pressures secondary to air-trapping. Thoracic ultrasonography can identify pneumothorax, pericardial effusion, or signs of elevated right ventricular systolic pressures (RV:LV, septal flattening).
  4. Assuming adequate intra-vascular volume is arriving at the left ventricle, rapid echocardiography can be used to provide a gross estimate of cardiac contractility and point to a cardiogenic process. If there is no obvious pump failure, auscultation may reveal murmurs that would suggest systolic output is refluxing to lower-resistance routes (ex. mitral insufficiency, aortic insufficiency, or ventricular septal defect).
  5. Finally, if the heart rate is suitable, volume deficits are not grossly at fault, no obstructive process is suspected, and cardiac contractility is adequate and directed appropriately through the vascular tree, the cause may be distributive. Physical examination may reveal dilated capillary beds and low systemic vascular resistance.

Algorithm for the Evaluation of Hypotension

References

  1. Morchi R. Diagnosis Deconstructed: Solving Hypotension in 30 Seconds. Emergency Medicine News. 2015.

Altitude and Dysbarism

Altitude Illness

  • Risk factors: altitude, rapidity of ascent, sleeping altitude
  • Pathophysiology
    • Hypobaric hypoxia
      • Pulmonary: vasoconstriction  pulmonary hypertension capillary leak
      • Cerebral: vasodilation edema
    • Acclimatization
      • Hyperventilation primary respiratory alkalosis compensatory metabolic acidosis
      • Acetazolamide promotes renal bicarbonate excretion and accelerates acclimatization
  • Management: oxygen and descent

Acute mountain sickness (2000m)

  • Mild cerebral edema
  • Symptoms: headache, nausea/vomiting, fatigue (hangover)
  • Management: acetazolamide 250mg PO BID, dexamethasone 4mg q6h

High-altitude pulmonary edema (HAPE, 3000m)

  • Non-cardiogenic pulmonary edema
  • Symptoms: dyspnea at rest, cough, fever
  • Signs: hypoxia, crackles
  • CXR: patchy infiltrates
  • Management: nifedipine, PDEi (sildenafil), HBO

High-altitude cerebral edema (HACE, 4500m)

  • Cerebral edema
  • Symptoms: ataxia, altered mental status
  • Management: acetazolamide 250mg PO BID, dexamethasone 10mg then 4mg q6h, HBO
  • Gamow bag: portable HBO

Dysbarism (diving pathology)

  • Principles
    • Boyle’s Law: volume = 1/pressure
      • Volume changes greatest near surface
    • Henry’s Law: increased pressure increases proportion of dissolved gas

Barotrauma

  • Localized (descent)
    • Barotitis media
      • Mechanism: unequal pressure between external and middle ear.
      • Symptoms: pain, vertigo if ruptured
    • Barotitis externa
      • EAC edema/hemorrhage
    • Barotitis interna
      • Bleeding/rupture of round window
      • Symptoms: vertigo, tinnitus, hearing loss
      • Management: ENT referral
    • Sinus squeeze: pain and epistaxis
    • Mask squeeze: periorbital petechiae
  • Localized (ascent)
    • Barodontalgia
      • Air trapped in filling
      • Symptoms: pain, fracture
    • Alternobaric vertigo: Unequal ear pressure causing vertigo
    • GI barotrauma: belching, flatulence
  • Pulmonary overpressurization (ascent)
    • Mechanism: rapid ascent without exhalation, focal alveolar rupture leading to pneumomediastinum, rarely pneumothorax
    • CXR: continuous diaphragm sign
    • Symptoms: dysphonia, neck fullness, chest pain
    • Management: supportive
  • Air gas embolism (ascent)
    • Mechanism: similar to POP, air enters pulmonary venous circulation
    • Symptoms: MI, arrest, stroke, seizure within 10 minutes
    • Management: IVF, oxygen, HBO

Dissolved Gas Problems

  • Nitrogen narcosis
    • At >100ft, nitrogen enters nervous system and acts similarly to general anesthetic
    • Symptoms: similar to alcohol intoxication, complications arise from poor judgement
    • Management: ascent
  • Oxygen toxicity
    • Setting: industrial dives, deep
    • Symptoms: seizure, nausea, muscle twitching
  • Decompression sickness
    • Mechanism: nitrogen gas dissolves poorly in solution, with ascent forms bubbles, occurs 1-2 hours after ascent
    • Types
      • Musculoskeletal, integumentary (“bends”)
        • Symptoms: arthralgia, cutis marmorata
      • Neurological
        • Lower spinal cord (thoracic/lumbar/sacral)
          • Symptoms: paraplegia, paresthesia, bladder dysfunction
        • Cerebellum (“staggers”)
          • Symptoms: ataxia
        • Pulmonary (“chokes”)
          • Symptoms: similar to pulmonary embolus
        • Management: IVF, oxygen, HBO

Bites

Mammalian

  • Human: Eikenella corrodens
  • Dog/Cat: Pasteurella multocida

Athropod

  • Hymenoptra (bee, wasp, hornet, ant)
    • Venom: histamine reaction, anaphylaxis
    • Symptoms
      • Local: pain, swelling, pruritus
      • Toxic (<48h): multiple bits, N/V, syncope, HA
      • Anaphylaxis: minutes
      • Delayed (10-14d): serum sickness, fever, arthralgia, malaise
    • Management
      • Remove stinger
      • Wash, ice, anti-histamine, analgesia
  • Brown recluse (violin pattern)
    • Location: Midwest, wood pile
    • Symptoms: initially painless, cytotoxic venom may cause necrosis
    • Management: supportive, Tdap, delayed debridement if necrotic
  • Black widow (red hourglass)
    • Venom: neurotoxic, ACh, NE
    • Symptoms: painful, erythema, muscle contractions (“acute abdomen”), localized diaphoresis from ACh release
    • Management: analgesia, benzodiazepines, antivenom for refractory pain (may cause anaphylaxis)

Snake

  • Crotalid (rattlesnake, copperhead, cottonmouth, collectively “pit vipers”)
    • Venom: cytotoxic, hemorrhagic
    • Symptoms: erythema/edema (ecchymoisis/bullae), nausea/vomiting, metallic taste
    • Labs: DIC
    • Management
      • Immobilization (no tourniquet)
      • Local wound care, Tdap
      • CBC, INR, fibrinogen (q2h)
      • Antivenom (Crofab 4-6 vials): given until symptoms or laboratory abnormalities arrest
      • Compartment syndrome: avoid surgery
  • Elapidae (coral snake, “red on yellow”)
    • Venom: neurotoxic, delayed 10-12h
    • Symptoms: no significant local reaction, bulbar palsies, respiratory depression
    • Management: no antivenom, supportive care, intubation

Cnidaria (jellyfish)

  • Symptoms: local pain, erythema, pruritus
  • Management: 5% acetic acid, alcohol, remove stinger
    • Antivenom for box jellyfish

Stingray

    • Symptoms: local pain, edema
    • Management: Local wound care, Tdap, hot water immersion, antibiotics for Vibrio (cephalexin with doxycycline)

Vibrio vulnificus

  • Symptoms: necrotizing fasciitis, in cirrhotic primary septicemia after ingesting shellfish

Electrical Injuries

 

Physics

  • High-voltage defined as >1,000V
  • Voltage related to injuries current via resistance (V=IR)
  • AC is 3x more lethal than DC
    • Fluctuation at 60Hz causes tetany, maintained grasp on source

Effects

  • Dysrhythmia
    • DC: asystole
    • AC: ventricular fibrillation
    • Delayed dysrhythmia uncommon
  • Burn
  • Tissue ischemia: vascular spasm or thrombosis
  • CNS: AMS, seizure, ICH, neuropathy
  • MSK: posterior shoulder dislocation

Management

  • Asymptomatic: None
  • Mild (i.e. small burn): ECG, UA (rhabdo)
  • High voltage: Labs, CT, admit for observation
  • Pediatrics: oral commissure burn, discharge with plastic surgery follow-up if no LOC, normal ECG, tolerating PO. Risk of delayed labial artery bleeding.

Complications

  • Keraunoparalysis: current travels up and down lower extremities causing transient paresthesia and paralysis.
  • Trauma: TM rupture, other mechanical injuries

 

Heat Emergencies

Overview

  •  Spectrum
    • Cramps
    • Syncope
    • Exhaustion
    • Stroke
  • Physiology of cooling
    • Radiation: body warmer than environment, heat radiates away
    • Evaporation: environment warmer than body, sweat promotes heat exchange, affected by ambient humidity

Heat cramps

  • Mechanism: fluid/electrolyte depletion resulting in muscle cramps
  • Management: IVF, electrolyte repletion, cooling

Heat syncope

  • Mechanism: vasodilation resulting in hypotension
  • Management: IVF, cooling, rule out alternative etiologies

Heat exhaustion

  • Mechanism: similar to heat cramps
  • Symptoms: influenza-like, headache, fatigue, dizziness, nausea, normal mental status distinguishes from heat stroke
  • Findings: temperature <40°C
  • Management: IVF, cooling

Heat stroke

  • Mechanism: similar to heat cramps
  • Symptoms: prodrome of heat exhaustion
  • Signs: AMS, ataxia, seizure
  • Findings: temperature >40°C
  • Mortality: 30-80%
  • Labs: AST/ALT, coagulopathy, DIC, rhabdomyolysis, ATN/AKI
  • CXR: pulmonary edema
  • Types
    • Classical: elderly, dry skin, mild dehydration, increased mortality
    • Exertional: young athlete, diaphoretic, increased morbidity (organ failure)
  • Management
    • Evaporative cooling
    • Ice packs to large vessels
    • GI lavage
    • Liberal intubation
    • Benzodiazepines or thorazine for inappropriate thermogenesis (shivering)
    • Halt cooling at 40°C

Hypothermia

Overview

  • Risk factors
    • Extremes of age
    • Behavioral: psychosis, intoxication
  • Types
    • Chillblains
    • Immersion foot
    • Frostnip
    • Frostbite
    • Generalized

Hypothermia

Chilblains

  • Findings: red/white plaques on extremities
  • Symptoms: pruritus, pain
  • Management: supportive (gentle warming), topical corticosteroids, consider nifedipine

Immersion foot (trench)

  • Mechanism: prolonged immersion in non-freezing water, vasoconstriction leads to ischemia/necrosis
  • Findings: pale, mottled skin, paresthesia
  • Management: supportive, drying and rewarming
  • Complications: gangrene

Frostnip

  • Retrospective distinction from frostbite after rewarming if no tissue loss

Frostbite

  • Mechanism: extracellular then intracellular crystal formation (mechanistically similar to crush injury)
  • Reperfusion: cellular injury triggers cytokine release upon reperfusion, results in microvascular thrombosis and tissue ischemia/necrosis
  • Classification: grades I-II superficial to dermis, grades III-IV involve subcutaneous tissue to bone
  • Management
    • Rapid rewarming (immersion in warm water at 41°C)
    • Tdap
    • Debridement of clear blisters

Generalized

  • Causes
    • Exposure
    • Metabolic (adrenal, thyroid, hypoglycemia)
    • Sepsis
  • Grading
    • Mild (32.2-35°C)
      • Findings: excitation, tachycardia, hypertension, shivering thermogenesis
    • Moderate (30-32.2°C)
      • Findings: ataxia, AMS, bradycardia, hypotension, bradypnea
      • ECG:  Osborn wave
    • Severe (<30°C)
      • Complications
        • Increased risk of arrhythmia (bradycardia, slow atrial fibrillation, ventricular fibrillation, asystole)
        • Irritable myocardium
        • Decreased enzymatic activity
          • Renal: cold diuresis
          • Heme: coagulopathy (hidden on labs as blood rewarmed prior to testing)
          • Metabolic: hyperglycemia as insulin ineffective
      • Management
        • Ventricular fibrillation: attempt one shock, then focus on rewarming if ineffective
        • Goal >30°C

Radiation Exposure

Physics

  • Units
    • Gray (amount of radiation absorbed by body)
    • Sievert (toxicity associated with radiation exposure)
  • Types
    • Alpha: 0.1mm penetration, injury through ingestion
    • Beta: 1cm penetration, injury through skin or ingestion
    • Gamma: deep penetration
  • Factors
    • Time and distance (1/d2)
    • Shielding
    • Radiosensitive cells (rapidly dividing such as hematopoetic, GI)

Injury

  • Localized: epilation or burns, delayed by days
  • Internal (inhaled, ingestion)
    • Radioactive iodine: high dose results in thyroid ablation, low dose increases risk of thyroid malignancy
  • External: managed by removing clothing, soap/water shower
  • Whole body (gamma)
System Dose Time of onset Signs/Symptoms
Hematopoetic 2G 2d Pancytopenia, increased risk of infection
GI 6G Hours Nausea/vomiting, diarrhea, GI bleeding
CV/CNS 10G Minutes Shock, seizure

Key clinical features

  • Multiple affected individuals with nausea/vomiting suggests radiation exposure
  • Rapidity of onset of symptoms suggests increased dose/exposure
  • LD505G
  • Prognosis by lymphocyte count
    • ALC >1000 at 48h suggests good prognosis
    • ALC <300 at 48h suggests poor prognosis

Submersion Injury

Pathophysiology

  • Breath-holding until eventual involuntary gasp which triggers reflexive laryngospasm. Resultant loss of consciousness may cause laryngeal relaxation and aspiration.
  • Fluid aspiration results in decreased surfactant activity and atelectasis. This is complicated by V/Q mismatch and atelectrauma which can lead to ARDS.

Symptoms

  • Progressive respiratory distress
  • AMS: due to cerebral hypoxia
  • Shock: uncommon, consider trauma

Management

  • Albuterol
  • BiPAP
  • Endotracheal intubation
  • ECMO

Disposition

  • Asymptomatic or minor event: observe 2-3 hours
  • Mildly symptomatic: observe 4-6 hours
  • Hypoxia: admit
  • PPV: ICU

Toxicology

Drugs of Abuse

Synthetic Cannabinoids (Spice, K2)

  • Symptoms: anxiety, paranoia, tachycardia
  • Unique symptoms compared to traditional cannabinoids: psychosis, seizure, diaphoresis

Hallucinogenic amphetamines (ecstasy, MDMA)

  • Increased serotonergic activity
  • Management: supportive care (IVF, cooling for hyperthermia), benzodiazepines

Gamma-hydroxybutyrate (GHB)

  • Symptoms: euphoria, hypersexuality, rapid onset/clearance
  • Signs: bradycardia, bradypnea, coma with rapid awakening
  • Management: intubation for depressed GCS
  • Withdrawal: symptoms and treatment identical to ethanol withdrawal, consider baclofen

Cathinone (bath salts)

  • Symptoms: hallucinations
  • Signs: tachycardia, hypertension, tremor, mydriasis, diaphoresis, hyperthermia, bruxism
  • Management: benzodiazepines, consider paralysis, avoid beta-blockers

Cocaine

  • MOA: increase catecholamines, Na-channel blockade
  • Toxicity: HTN, tachycardia, hyperthermia, rhabdomyolysis, MI, seizure, VT
  • Management: benzodiazepines, cooling, anti-hypertensives (nitrate, CCB, not B-blocker)

Amphetamine

  • Toxicity: HTN, tachycardia, hyperthermia, rhabdomyolysis, intracranial hemorrhage
  • Management: same as cocaine

Benzodiazepines

  • Toxicity: sedation, respiratory depression
  • Management: consider flumazenil 0.2mg IV q1min x1-5

Toxic Alcohols

  • Overview
    • Toxic metabolites produced by alcohol dehydrogenase which can be inhibited by ethanol or fomepizole
    • Fomepizole: 15mg/kg loading dose, 10mg/kg q12h x4 doses then 15mg/kg q12h (stimulates own metabolism); if dialysis, q4h
  • Diagnosis: osmolar gap (>14), 2Na + Glu/18 + BUN/2.8 + EtOH/4.6
  • Treatment
    • ADH inhibition
    • HCO3
    • Hemodialysis
    • Supportive care
    • Hypoglycemia: dextrose

Methanol

  • Component of antifreeze, windshield washer fluid
  • Metabolite formic acid which causes acidosis and blindness
  • Can give folate

Ethylene glycol

  • Component of antifreeze, automobile coolants, de-icing agents
  • Metabolite oxalic acid which precipitates calcium oxalate crystals and causes acute renal failure
  • Can give thiamine (100mg q6h), pyridoxine (500mg q6h), Mg

Isopropanol

  • Component of rubbing alcohol
  • Metabolite acetone which does not cause acidosis

Analgesics

Acetaminophen

  • Metabolism: glucoronidation, CYP450
    • CYP450 pathway produces toxic metabolite when glucoronidation overwhelmed
    • In pediatrics, sulfation process protective
  • Toxic dose: >150mg/kg, >3g/day
  • Injury: liver (centrilobular necrosis), renal, pancreatic
  • Increased risk: induced CYP450 (chronic EtOH, rifampin, anti-epileptics)
  • Nomogram: applicable to single ingestion at 4-hours
  • Labs: PT/INR, LFT, lipase, chemistry
  • Management: NAC
    • PO: 140mg/kg, 70mg/kg q4h
    • IV: 150mg/kg, 50mg/kg over 4h, 100mg/kg over 16h

NSAID

  • Symptoms
    • Acute: GI upset, low risk UGIB
    • Acute massive: acidosis, coma, seizures
    • Chronic: UGIB, nephropathy, agranulocytosis

Aspirin

  • Signs: tachycardia, hyperthermia, tachypnea/hyperpnea
  • Severe: cerebral and pulmonary edema, CNS hypoglycemia
  • Labs: primary respiratory alkalosis with metabolic acidosis
  • Management
    • Hypoglycemia (CNS) treatment
    • Bicarbonate infusion (urine pH > 8)
    • Hemodialysis for pulmonary edema, cerebral edema, renal failure, acidemia, level >100mg/dL (acute) or > 60mg/dL (chronic)

Opioids

  • Symptoms: respiratory depression, miosis
  • Management: naloxone 0.04mg, 0.4mg, 2mg
  • Withdrawal: nausea/vomiting, diarrhea, abdominal pain, piloerection
    • Neonates: seizure, death
  • Complications with specific agents:
    • Meperidine, tramadol: seizures
    • Methadone: QT prolongation

Anesthetics

Lidocaine

  • Mechanism: Na-channel blockade
  • Types:
    • Ester (one “i”): cocaine, procaine, benzocaine
    • Amide (two “i”): lidocaine, bupivacaine
  • Toxicity
    • Dose: 4mg/kg, 7mg/kg with epinephrine
    • CNS: perioral numbness, slurred speech, seizure
    • CV: VT, VF, AV block
    • Methemoglobinemia: methylene blue
  • Treatment
    • Seizure management
    • Bicarbonate for dysrhythmia
    • Intralipid

Anti-cholinergics

Sympathetic Parasympathetic
Mydriasis Miosis
Bronchodilation Bronchospasm/bronchorrhea
Tachycardia Bradycardia
Urinary retention Urinary incontinence
Hyperglycemia Salivation/lacrimation
Diaphoresis Increased GI motility
  • Examples
    • Atropine
    • Anti-histamine
    • TCA
    • Phenothiazines
    • Jimson weed
  • Symptoms
    • Peripheral: mydriasis, anhidrosis, flushing, hyperthermia, ileus, dry mucous membranes, AUR
    • Central: agitation (passive), delirium, coma, seizure
  • Treatment
    • Supportive
    • Benzodiazepines
    • Theoretically physostigmine
      • Avoid in seizure, QRS-widening, reactive airway disease
      • Possible diagnostic use

Drugs causing miosis (COPS)

  • C: cholinergics
  • O: opioids
  • P: phenothiazines
  • S: sedatives

Drugs causing QT-prolongation

  • Examples:
    • Phenothiazines
    • Anti-arrhythmics
    • Butyrophenones (ex. haloperidol)
    • Macrolides
    • Fluoroquinolones
    • Methadone
    • Ondansetron
    • Atypical antipsychotics
  • Treatment
    • Magnesium sulfate 2g IV over 1min
    • Overdrive pacing (transcutaneous, transvenous if not captured)
    • Consider isoproterenol (pharmacologic overdrive)

Serotonin syndrome

  • Cause: exposure to serotonergic agent(s)
  • Symptoms: agitation, mydriasis, tremor/clonus in lower extremities, tachycardia, hyperthermia
  • Management
    • Supportive care (IVF, vasopressors)
    • Cooling measures and paralysis for hyperthermia
    • Benzodiazepines
    • Cyproheptadine 12mg PO/NG
    • Dexmedetomidine infusion

Anti-emetics

Phenothiazines

  • Examples: compazine (prochlorperazine), phenergan (promethazine)
  • MOA: DA-antagonist
  • AE: sedation, dystonia, parkinsonism
  • Toxicity: seizure, VT, hypotension (TCA-like)

5-HT3 antagonists

  • Examples: zofran (ondansetron), granisetron
  • Toxicity: QT-prolongation

Anti-hypertensives

Calcium channel blockers

  • Toxicity: hypotension, bradycardia, AV blockade, hyperglycemia
  • Management
    • Atropine: 0.5mg IV q2-3min
    • Glucagon: 5mg IV q10min x2 (with anti-emetic)
    • IVF, vasopressors (norepinephrine, epinephrine)
    • Calcium: 3g gluconate, 1-3g chloride
    • High-dose insulin: 1 unit/kg, monitor hypoglycemia/hypokalemia
    • Intralipid: 1.5mL/kg bolus then 0.25mL/kg/minute
    • GI decontamination
    • Pacing, IABP, ECMO

Beta blockers

  • Toxicity: similar to CCB, hypoglycemia
  • Management: similar to CCB, calcium ineffective

Digoxin (foxglove, oleander)

  • MOA: inhibits Na/K ATPase, increases intracellular calcium (inotropic)
  • Toxicity
    • CV: bradycardia, hypotension
    • ECG: bidirectional VT, PVC, scooped ST-segment
    • CNS: agitation, psychosis
    • Visual: yellow-green vision, halo
    • Metabolic: hyperkalemia (acute), hypokalemia, hypomagnesemia
  • Treatment
    • GI decontamination
    • Atropine
    • Transcutaneous pacing (avoid transvenous, irritable myocardium)
    • Digibind
    • Avoid calcium

Clonidine

  • Toxicity: bradycardia, hypotension, opioid mimic (miosis, lethargy, respiratory depression)
  • Management: supportive care, stimulation for respiratory depression, atropine

Sodium-channel blockers

  • Drugs
    • TCA
    • Diphenhydramine
    • Procainamide
    • Carbamazepine
  • ECG
    • QRS prolongation
    • Prominent “R” in aVR
    • RAD
  • Treatment
    • Sodium bicarbonate

Anti-hyperglycemics

Sulfonylurea

  • Symptoms: recurrent severe hypoglycemia
  • Management: octreotide 50-75mcg SQ/IM q6h

Other agents that cause hypoglycemia

  • EtOH
  • B-blocker
  • Quinine
  • Salicylate

Environmental

Carbon monoxide

  • Source: combustion (gas heater, indoor barbeque)
  • Toxicity
    • General: influenza-like, multiple proximate affected individuals
    • GI: abdominal pain, nausea
    • CNS: headache, dizziness, confusion, ataxia, seizure
    • CV: palpitations, arrhythmia, hypotension, MI
  • Treatment
    • T½: RA 6h, NRB 1h, 3atm 0.5h
    • Hyperbaric: neuro deficit, syncope, pregnancy, CV toxicity

Cyanide

  • Mechanism: inhibits oxidative phosphorylation
  • Source: structural fire (wool, silk)
  • Symptoms: syncope, seizure, coma, cardiovascular collapse
  • Detection: severe lactic acidosis, “arterialization” of venous blood, “bitter almond” odor
  • Treatment
    • Hydroxycobalamin (Cyanokit): 5g IV, may repeat x1
    • Sodium thiosulfate 12.5g IV

Methemoglobinemia

  • Mechanism: Fe2+ converted to Fe3+, “functional anemia”
  • Source: nitrite (food), topical/local anesthetics, pyridium, dapsone, reglan
  • Detection: normal PaO2, SpO2 85% unresponsive to supplemental oxygen, ABG with co-oximetry
  • Management: methylene blue 1-2mg/kg IV if symptomatic or MetHb >25%
    • Contraindicated in G6PD deficiency, treat with exchange transfusion or HBO

Hydrogen Sulfide

  • Source: industrial, sulfur spring, sewer
  • Detection: “rotten egg” odor
  • Management: remove from source, supportive care

Hydrocarbon

  • Source: huffing canisters
  • Toxicity: VT/VF from myocardial sensitization
  • Management: beta-blockade
  • Complications: harmless if ingested, aspiration leads to ARDS

Hydrofluoric acid

  • Source: rust remover, wheel cleaner, glass etching
  • Symptoms: pain-out-of-proportion, delayed onset
  • Toxicity: Hypocalcemia (QTc prolongation, VT/VF/TdP), hyperkalemia, hypomagnesemia
  • Management: analgesia, topical calcium gluconate gel, intravenous calcium for large BSA involvement

Alkaline ingestion

  • Symptoms: esophageal perforation, delayed stricture

Acid ingestion

  • Symptoms: gastric perforation (rare), delayed gastric outlet obstruction
  • Findings: metabolic acidosis

Botulism

  • Sources
    • Adult: ingested preformed toxin
    • Infants: ingested spores (achlorhydric), in vivo toxin production
    • Wound: black tar heroin
  • Symptoms: dysphagia, ptosis, diplopia, respiratory failure, descending paralysis
    • Infants: constipation, floppy
  • Management: supportive care, intubation
    • Adults: Anti-toxin from CDC or local Department of Health
    • Infants: 100mg/kg IV x 1 dose (BabyBIG)

Heavy Metals

Iron

  • Dose
    • Ferrous sulfate: 20% elemental iron
    • Toxic: >20mg/kg
    • Lethal: >60mg/kg (1 tablet 325mg ferrous sulfate per kilogram)
  • Toxicity: corrosive, anti-coagulant, hepatotoxic
  • Course
    • Stage I: GI effects, emesis with hematemesis
    • Stage II: Quiescent
    • Stage III: Systemic, multi-organ system dysfunction
    • Stage IV: Resolution, gastric scarring and outlet obstruction
  • Workup
    • CBC/BMP
    • LFT
    • Lactate
    • Fe level
    • KUB (if positive consider WBI)
  • Treatment
    • Decontamination: no activated charcoal, consider WBI
    • Deferoxamine: 15mg/kg/hr

Lead

  • Source: paint, batteries
  • Toxicity
    • Acute: headache, encephalopathy, seizure
    • Chronic: malaise, weight loss, arthralgia, anemia (basophilic stippling)
  • Diagnosis: lead level, wrist drop
  • Management: chelation (BAL, EDTA, DMSA) for level >50ug/dL or asymptomatic >70ug/dL

Lithium

  • Source: iatrogenic, drug-drug interaction
  • Symptoms
    • GI: nausea/vomiting, diarrhea
    • CNS: tremor, coma
    • CV: TWI, QT-prolongation
  • Management
    • IVF, encourage renal elimination
    • Hemodialysis

Other Drugs

Disulfuram

  • MOA: aldehyde dehydrogenase inhibitor
  • Symptoms: increased acetaldehyde leads to flushing, headache, nausea/vomiting, tachycardia, hypotension
  • Management: antihistamine, IVF, vasopressors
  • Other agents causing disulfuram-like reaction: metronidazole, INH, sulfonylurea

Isoniazid

  • Toxicity: seizure
  • Management: pyridoxine 5g IV, repeat x1

Theophyline

  • Toxicity: seizure
  • Management
    • Decontamination: AC
    • Seizures: benzodiazepines
    • Tachyarrhythmia (commonly MAT): beta-blockade
    • Hemodialysis: acute > 100mg/L, chronic >30mg/L

Monoamine oxidase inhibitors

  • Toxicity: food/drug interaction
  • Symptoms: tachycardia, hypertension, hyperthermia, agitation
  • Management: cooling, IVF, management of hyper/hypotension

Phenytoin

  • Oral: cerebellar dysfunction (ataxia), CNS depression
  • IV: hypotension (suspension contains propylene glycol)

Nutritional Supplements

  • Fat-soluble vitamins
    • A: benign intracranial hypertension
    • D: hypercalcemia

Envenomations

Snake

  • Crotalid (rattle), elapidae (coral)
  • Symptoms
    • Local reaction: edema, hemorrhagic bullae
    • Systemic: perioral numbness, fasciculations
    • Severe: thrombocytopenia, decreased fibrinogen
  • Management: Crofab 5 vials

Spider

  • Black widow
    • Identification: hourglass on abdomen
    • Symptoms: painful bite, target-appearance, rarely “acute abdomen”
    • Management: analgesia, anti-venom, tetanus
  • Brown recluse
    • Identification: violin shape on head
    • Geography: Southeast, Midwest
    • Symptoms: painless bite, local reaction, delayed healing with eschar
    • Rare: hemolysis, DIC, shock
    • Management: supportive care, antibiotics if superinfected, consider dapsone, tetanus

Scorpion (Centruroides)

  • Geography: Arizona
  • Symptoms
    • Autonomic: HTN, tachycardia, diaphoresis
    • CNS: opsoclonus, slurred speech, dysphagia
  • Management: anti-venom, supportive care, analgesia, tetanus

Marine

  • Ciguatera
    • Source: toxin bioconcentrated in fish
    • Symptoms: gastroenteritis, hot/cold-reversal, “loose teeth” sensation
    • Management: mannitol
  • Scombroid
    • Source: poorly-refrigerated fish, histamine-like
    • Symptoms: flushing trunk/face (distinguish from allergic reaction), gastroenteritis
    • Management: supportive care, IVF, anti-histamine, bronchodilators if indicated
  • Paralytic shellfish poisoning
    • Source: bivalve
    • Symptoms: gastroenteritis, paralysis
    • Management: supportive, intubation
  • Jellyfish and Cnidaria
    • Source: nematocyst
    • Symptoms: burning pain, pruritus
    • Severe: Irakundji syndrome (HTN, pulmonary edema)
    • Management: supportive, analgesia, box jellyfish antidote, consider vinegar
  • Stingray
    • Source: heat-labile toxin
    • Management: affected area in warm water, tetanus, ciprofloxacin (Vibrio)

Mushrooms

  • Amanita: centrilobular necrosis, similar to acetaminophen
  • Gyronatum: similar to INH (seizure and treatment), may cause methemoglobinemia
  • Symptoms: muscarinic (SLUDGE)
    • Early onset generally benign, delayed onset (>6h) suggests more serious course
  • Management: atropine, glycopyrrolate, IVF

Pesticides

  • Organophosphate: irreversible
  • Carbamate: reversible
  • Symptoms: muscarinic (SLUDGE)
  • Treatment: atropine 2-6mg IV double q5min to control secretions, pralidoxime (for organophosphates)

Strychnine

  • Source: rodenticide
  • Symptoms: myoclonus, opisthotonus, agitation
  • Management: benzodiazepines, airway protection, paralysis

Atypical Antipsychotic Overdose

History & Physical

38M, unknown medical history, brought in after being found unresponsive next to an empty bottle of Seroquel. Presenting vital signs notable for blood pressure of 96/43, heart rate 103. Examination reveals tentatively protected airway (GCS E2 M5 V3, SpO2 100%, RR 14), normal pupil diameter and reactivity, dry mucous membranes with thick vomitus in oral cavity.

Laboratory evaluation was unremarkable, and there was no evidence of aspiration on chest radiography. ECG showed sinus tachycardia without QT prolongation. Blood pressure increased to normal range with fluid resuscitation. The patient’s mental status progressively improved and he was discharged after six hours of uneventful continuous cardiac monitoring.

Toxidrome Summary1

Class Vital Signs Mental Status Pupils Skin Other Examples
Anti-cholinergic T
HR
BP
Delirium
Agitation
Coma
Mydriasis Dry Urinary retention
BS
Anti-histamines
Anti-parkinson
Anti-psychotic
Anti-depressant
Sympathomimetic T
HR
BP
Agitation
Hallucination
Paranoia
Mydriasis Diaphoresis Tremor
Hyperreflexia
Cocaine
Amphetamine
Ephedrine
Opioid/Sedative HR
RR
BP
CNS depression
Coma
Miosis   Hyporeflexia
Needle marks
Opioids
Benzo
Barbiturates

Evaluation1,2

  • POC Glucose
  • ECG (QT interval)
  • Serum acetaminophen, salicylate, EtOH level
  • Serum drug levels if known (anti-epileptics)
  • Urine toxicology screen
  • Chemistry (metabolic acidosis, electrolytes, renal function)
  • LFT (hepatotoxicity)
  • CK (rhabdomyolysis)
  • Serum osmolarity (osmolar gap)
  • UA with microscopy (crystals in ethylene glycol poisoning)
  • ABG (carboxyhemoglobin, methemoglobin)

Pharmacology, Toxicity and Management of Second Generation Antipsychotic (SGA) Overdose3

Pharmacology, Toxicity and Management of Second Generation Antipsychotic (SGA) Overdose

References

  1. Kulig, K. (2013). General Approach to the Poisoned Patient. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 1954-1959). Elsevier Health Sciences.
  2. Wittler, M., & Lavonas, E. (2013). Antipsychotics. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 2047-2051). Elsevier Health Sciences.
  3. Levine M, Ruha A-M. Overdose of atypical antipsychotics: clinical presentation, mechanisms of toxicity and management. CNS Drugs. 2012;26(7):601–611.
  4. WikEM: Antipsychotic toxicity

Acute Diarrhea (in developing countries)

A clinic near JalapaHPI:

1yo M, ex-term, previously healthy, with 8d tactile fever/diarrhea, initially watery, presenting now due to bloody diarrhea x1d. Mother reports 8-10 episodes/day, decreased PO intake and urine output x4d and changes in behavior (lethargy, irritability). No vomiting, no e/o abdominal pain, no cough, no seizures, no weight loss, no known sick contacts.

PMH:

  • Full term
  • No perinatal complications
  • Vaccination history unknown

SHx:

  • Meeting all developmental milestones
  • No sick contacts

PSH/FH/Meds/Allergies:

None

Physical Exam:

  • VS:   HR 135    BP 86/60    RR 24    T N/A    Wt 11kg (60%)
  • General: Patient was initially examined after initial rehydration with IVF. Well-appearing child, interactive and smiling.
  • HEENT: NC/AT, PERRL, MMM no lesions, no nuchal rigidity
  • CV: RRR, normal S1/S2
  • Lungs: CTAB
  • Abd: +BS, soft, NT/ND, no rebound/guarding
  • Ext: Warm, well-perfused, 2+ peripheral pulses (radial, DP, PT), capillary refill <2s
  • Skin: No visible skin lesions
  • Neuro: Alert and responsive

Assessment/Plan:

1yo healthy male with fever, bloody diarrhea and history consistent with dehydration. Most likely cause of acute diarrhea in this patient is infectious, particularly Shigella spp given presence of blood. Other concerning causes of diarrhea in this patient with reports of fever and changes in mental status include a serious bacterial illness (meningitis, pneumonia, UTI), however, these are less likely given the predominant, voluminous diarrhea and absence of symptoms associated with each. Other considerations include appendicitis, volvulus, intussusception, however again copious diarrhea in association with a benign abdominal exam makes these causes less likely. Early presentation of chronic diarrhea cannot be ruled out, however unlikely given association with fever and local prevalence of infectious causes.

Management included IV rehydration, followed by maintenance with PO ORS, early nutritional support, and ciprofloxacin 15mg/kg IV q12h.

Types and causes of acute diarrhea: 1, 2

Types and Causes of Acute Diarrhea

Assessment of Hydration Status

 

Dehydration Level

Variable/Sign Mild (3-5%) Moderate (6-9%) Severe (>10%)
General appearance Restless, alert Drowsy, postural hypotension Limp, cold, sweaty, cyanotic extremities
Radial pulse Normal rate, strength Rapid, weak Rapid, thready, sometimes impalpable
Respiration* Normal Deep Deep and rapid
Anterior fontanelle Normal Sunken Very sunken
SBP Normal Normal or low Low
Capillary refill* Normal (<2s) Prolonged (2-4s) Markedly prolonged (>4s)
Skin turgor* Normal Pinch retracts slowly Pinch retracts very slowly
Eyes Normal Sunken Grossly sunken
Tears Present Absent Absent
Mucous membranes Moist Dry Very Dry

* = sensitivity > 70% 3,4

Management of Acute Diarrhea: 5,6

Management of Acute Diarrhea

Pathogens causing diarrhea: 6

Pathogen Epidemiology/Transmission Comments Incubation Fever Abd. pain N/V Bloody stool Stool WBC Stool Heme
S. aureus, B. cereus Food poisoning with preformed toxin Vomiting > diarrhea 1-6h X X X X
C. perfringens Spores germinate in meats, poultry 6-24h X X X X
Norovirus Winter outbreaks in schools, nursing homes, cruise ships Adults: diarrhea

Children: vomiting

1-2d X X X
Rotavirus #1 MCC children Vaccine available 1-2d X X X
Campylobacter #1 MCC invasive enterocolitis in US

Undercooked poultry

GBS 2-5d
Salmonella #2 MCC enterocolitis in US Outbreaks

Undercooked egg, dairy, poultry

1-3d
Shigella Community-acquired, person-to-person 1-3d
EIEC Outbreaks

Undercooked beef, raw seed sprouts

Produces Shiga toxin 1-8d
C. difficile Nosocomial Leukocytosis X
E. histolytica Travel to tropical regions
Giardia Day care, waterborne transmission 1-3d X X X X
Vibrio Contaminated water, seafood 1-3d
Yersinia Foodborne transmission Mesenteric lympadenitis (simulates acute appendicitis) 1-3d

References:

  1. Huilan, S., Zhen, L. G., Mathan, M. M., Mathew, M. M., Olarte, J., Espejo, R., Khin Maung, U., et al. (1991). Etiology of acute diarrhoea among children in developing countries: a multicentre study in five countries. Bulletin of the World Health Organization, 69(5), 549–555.
  2. Navaneethan, U., & Giannella, R. A. (2008). Mechanisms of infectious diarrhea. Nature clinical practice. Gastroenterology & hepatology, 5(11), 637–647. doi:10.1038/ncpgasthep1264
  3. Steiner, M. J., DeWalt, D. A., & Byerley, J. S. (2004). Is this child dehydrated? JAMA : the journal of the American Medical Association, 291(22), 2746–2754. doi:10.1001/jama.291.22.2746
  4. Gorelick, M. H., Shaw, K. N., & Murphy, K. O. (1997). Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics, 99(5), E6.
  5. Harris, JB, Pietroni M. Approach to the child with acute diarrhea in developing countries. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
  6. Thielman, N. M., & Guerrant, R. L. (2004). Clinical practice. Acute infectious diarrhea. The New England journal of medicine, 350(1), 38–47. doi:10.1056/NEJMcp031534

Gastosin Ingestion

Jalapa, NicaraguaCC:

“Gastosin” ingestion

HPI:

29F BIB family after patient was found down at home, near opened bottle of Gastosin in presumed suicide attempt. On arrival to ED, patient was awake, but unresponsive, groaning and clutching stomach. GCS  was E3-V2-M5, HR 110, BP 60/palp, RR 24.

ED Course:

Upon arrival, placed two large-bore IV w/rapid infusion of 2L NS and given DA 2g IV x2. NG tube placed, initiated lavage of gastric contents with NS. Patient’s mental status continued to deteriorate, became unresponsive.

PMH/PSH:

Unknown

SHx:

History of alcohol abuse and depression per family.

PE:

  • VS: 110bpm, 60/palp, 24 R/min, no temp/O2sat available
  • General: Ill-appearing female, laying on bed in considerable distress, groaning and clutching stomach, diaphoretic
  • HEENT: NC/AT, PERRL (4-3mm), EOMI, MMM no lesions, no tongue lacerations, breath with foul odor, TM’s clear b/l.
  • CV: RRR, normal S1/S2, tachycardia, faint heart sounds, JVP elevated though patient supine
  • Lungs: CTAB, no crackles/wheezes
  • Abdomen: +BS, soft, non-distended, no guarding, no ecchymosis
  • GU: Normal external genitalia, loss of stool noted.
  • Neuro: Patient confused, initially responsive to sternal rub, moving all 4 extremities spontaneously/equally, EOMI without nystagmus, gag reflex present, DTR 2+ and symmetric throughout with toes downgoing.
  • Extremities: Cool, peripheral pulses 0 (radial, PT, DP), 1+ (femoral, brachial, carotid)1, capillary refill 3sec
  • Skin: No visible skin lesions

Assessment & Plan:

29F, unknown PMH, ċ ingestion of unknown amount of “Gastosin”. Patient presenting in likely cardiogenic shock given hypotension with reflex sympathetic activation (evidenced by peripheral vasoconstriction à cool extremities, diaphoresis) and no evidence of hemorrhage. Gastosin is a pesticide used in the storage of maize2, and is well-known locally as a common agent in self-poisonings. Chemically composed of aluminum phosphide, and liberates phosphine gas on exposure to moisture which is rapidly absorbed by inhalation, transdermally or gastrointestinally. Toxicity results from free radical damage and inhibition of enzymes of metabolism (particularly affecting cardiac myocytes). Clinical features include vomiting, resistant hypotension and metabolic acidosis.3

Patient’s symptoms and presentation are consistent with cardiogenic shock secondary to Gastosin ingestion. Management included fluid resuscitation and inotropic support with dopamine, as well as gastric lavage. Resuscitation efforts were unsuccessful and patient remained hypotensive with worsening of mental status, and eventual death.

Differential Diagnosis for Shock:

A System for Shock

A System for the Management of Aluminum Phosphide Poisoning:4,5

Management of Aluminum Phosphide Poisoning

The Glasgow Coma Scale:

  Eye Opening Best Motor Response Best Verbal Response
1 None None None
2 Pain Extension Groans
3 Verbal Flexion Unintelligible
4 Open Withdraws Disoriented
5 Localizes Oriented
6 Obeys commands

References:

  1. Hill RD, Smith RB III. Examination of the Extremities: Pulses, Bruits, and Phlebitis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 30. Available from: http://www.ncbi.nlm.nih.gov/books/NBK350/
  2. Udoh, J., Ikotun, T., & Cardwell, K. (n.d.). Storage systems for maize (zea mays l.) in nigeria from five agro-ecological zones. Proceedings of the 6th International Working Conference on Stored-product Protection, 2, 960-965.
  3. Bogle, R. G., Theron, P., Brooks, P., Dargan, P. I., & Redhead, J. (2006). Aluminium phosphide poisoning. Emergency medicine journal : EMJ, 23(1), e3. doi:10.1136/emj.2004.015941
  4. Gurjar, M., Baronia, A. K., Azim, A., & Sharma, K. (2011). Managing aluminum phosphide poisonings. Journal of Emergencies, Trauma, and Shock, 4(3), 378–384. doi:10.4103/0974-2700.83868
  5. Jones, A. L., & Volans, G. (1999). Management of self poisoning. BMJ (Clinical research ed.), 319(7222), 1414–1417.