This section focuses on the aspects of acute poisoning that are potentially life threatening or may lead to permanent organ damage and hence require immediate, usually intensive, medical care. This has been organized into a table to facilitate rapid access to concise toxicology information guiding management of acutely poisoned patients. The table is divided into four columns. The first column is alphabetically organized into either a specific agent (e.g., acetaminophen) or a class of agent (e.g., alcohol) with specific toxins (e.g., ethylene glycol, isopropanol, and methanol); individual agents appear alphabetically in the index. This is followed by a list of organ systems that can be targeted by the agent or its systemic effects. The second column focuses on action alerts, critical laboratory values, guidelines for clinical intervention, and the dosing of therapeutic drugs, antidotes, or antivenom. The third column lists adjunct therapy and extracorporeal treatments. The fourth column highlights caveats and potential complications. The content of this section is not a substitute for reference textbooks in intensive care medicine or medical toxicology, and does not address envenomations that usually occur outside of the United States. The interested reader is referred to the current edition of Irwin and Rippe’s Intensive Care Medicine textbook and toxicology textbooks (e.g., Goldfrank’s Toxicologic Emergencies and Medical Toxicology) for more detailed information on a given subject.
TABLE 96-1
Agent Target Organ Systemic Effect
Action Alert Critical Laboratory Value Clinical Intervention
Adjunct Therapy Extracorporeal Support
Caveat Complication
Acetaminophen (APAP)
Acute:
GI
Hepatotoxicity
FHF
Neurologic
Encephalopathy
Coma and metabolic acidosis with serum APAP > 800 µg/mL (5,292 µmol/L) 4-12 h postingestion.
GU
Oliguric renal failure 24-48 h with proteinuria, microscopic hematuria and back pain; usually proceeded by hepatotoxicity; non-oliguric renal failure is rare.
Serum APAP concentration above “treatment” line on acetaminophen toxicity (Rumack-Matthew) nomogram (Fig. 96-1):
NAC
Oral: 140 mg/kg followed by 70 mg/kg every 4 h (dilute 3:1 with carbonated/fruit beverage for palatability); administer IV antiemetic (e.g., ondansetron 8 mg; Peds: 0.2 mg/kg, max 8 mg) and repeat the same oral dose if vomiting occurs within 1 h.
OR
IV: 150 mg/kg in 200 mL D5W over 1 h followed by 50 mg/kg in 500 mL D5W over 4 h followed by 100 mg/kg in 1 L D5W over 16 h (6.25 mg/kg/h).
NAC therapy may be terminated if the patient remains asymptomatic, serum APAP concentration below “treatment” line, and AST/ALT remains in the laboratory reference range at 20-24 h; continue NAC therapy (oral: every 4 h; IV 6.25 mg/kg/h) if patient’s clinical condition deteriorates or AST/ALT becomes abnormal.
APAP/NAC-induced emesis: IV ondansetron 8 mg (Peds: 0.2 mg/kg, max 8 mg); metoclopramide 1-2 mg/kg.
Encephalopathy or FHF: IV NAC with the final infusion rate (6.25 mg/kg/h) until recovery or death.
Transfer to liver unit/ICU consideration: PT (measured in seconds) exceeds the time in hours after overdose, or INR >5.0 at any time, or metabolic acidosis, hypoglycemia, or renal failure.
OLT consideration:
Consider listing for transplantation: Arterial lactate >3.5 mmol/L after fluid resuscitation.
List for transplantation: Arterial pH <7.30 and lactate >3.0 mmol/L after fluid resuscitation.
OR
PT/INR >100 s/>6.5, Cr >3.3 mg/dL (300 µmol/L), and encephalopathy grade ≥III within a 24-h period and normal arterial pH.
Unreliable time of ingestion
Patient with signs and symptoms consistent with hepatotoxicity: NAC treatment same as above; continue NAC treatment (oral: every 4 h; IV 6.25 mg/kg/h) until clear clinical and laboratory evidence of improvement in patient’s condition. If deterioration in clinical and laboratory status, consider parameters for referral to liver unit/ICU or OLT.
Asymptomatic patient with serum APAP concentration <10 mg/L (66 µmol/L) and AST/ALT within laboratory reference range: Repeat serum APAP level and AST/ALT in 6-8 h. If both normal, no further treatment for APAP overdose is needed. If either elevated, treat with NAC (same as above); NAC treatment may be terminated if the patient remains asymptomatic, serum APAP concentration <10 mg/L (66 µmol/L), and AST/ALT remains within or falls to the near upper limit of laboratory reference range at 20-24 h, otherwise continue NAC (oral: every 4 h; IV 6.25 mg/kg/h) until clear clinical and laboratory evidence of improvement or, if deterioration in clinical and laboratory status, consider parameters for referral to liver unit/ICU or OLT.
Consider oral activated charcoal 1-2 g/kg in a cooperative patient presenting within 4 h of overdose.
When to consider hemodialysis: Patient who present soon after an acute overdose, when NAC not available, no other options are available and hemodialysis can be expeditiously initiated; coma and metabolic acidosis with serum APAP >800 µg/mL (5,292 µmol/L); terminate when serum APAP <30 µg/mL (198 µmol/L) and acid-base disturbances are corrected.
The acetaminophen toxicity nomogram is valid following an acute single overdose of nonmodified release APAP occurring between 4 and 24 h; plots above “probable” and “high-risk” lines indicate 60% and 90% hepatotoxicity risk, respectively.
NAC therapy: Anaphylactoid reactions; infusion volume in pediatric patients.
Nonacute/repeated supratherapeutic ingestion: Same as Acetaminophen (APAP) “Acute”
Signs and symptoms consistent with hepatotoxicity: NAC treatment same as “Acute;” continue NAC until clear clinical and laboratory evidence of improvement; if deterioration in clinical and laboratory status, consider referral to liver transplant center (See acute ingestion section).
Asymptomatic patient with either serum APAP concentration >10 mg/L (66 µmol/L) or serum AST/ALT ≥50 IU/L: NAC treatment same as “Acute;” recheck laboratory tests for APAP, AST/ALT at the end of 12 h of NAC treatment; if serum APAP <10 mg/L (66 µmol/L) and serum AST/ALT <50 IU/L, terminate NAC treatment; otherwise, continue NAC treatment until serum APAP <10 mg/L (66 µmol/L) and serum AST/ALT <50 IU/L.
Asymptomatic patient with serum APAP concentration <10 mg/L (66 µmol/L) and AST/ALT <50 IU/L: No further treatment for APAP overdose is needed.
Same as “Acute,” except acetaminophen toxicity nomogram not valid at any time.
Serum bicarbonate <20 mmol/L or arterial pH <7.30: IV sodium bicarbonate 1-2 mmol/kg boluses, target blood pH 7.40, and urine pH 7.0-8.0.
Known or high index of suspicion of ingestion, clinical poisoning, or serum EG level ≥20 mg/dL (3.2 mmol/L):
IV 4MP 15 mg/kg followed by 10 mg/kg every 12 h × 4 doses, and then 15 mg/kg every 12 h thereafter until toxic alcohol is undetectable and clear clinical-biochemical recovery; all infusions over 30 min.
OR
IV ethanol (10% solution in D5W) 10 mL/kg over 1 h followed by 1.5 mL/kg/h, target serum ethanol 100 mg/dL until toxic alcohol is undetectable and clear clinical-biochemical recovery.
Maximize GFR: IV NS target urine output 2-4 mL/kg/h.
IV Pyridoxine 3-5 mg/kg/d or 50 mg every 6 h until toxic alcohol is undetectable and acidemia resolved.
IV thiamine 100 mg/d or every 6 h until toxic alcohol is undetectable and acidemia resolved.
Consider hemodialysis when serum EG ≥25 mg/dL (4.0 mmol/L) and acidemia or renal insufficiency.
4MP dosing: Administer the next scheduled dose if ≥6 h since last dose; during hemodialysis, dosing is every 4 h; end of dialysis and time of last dose 1-3 h administer half of next scheduled dose; >3 h administer next scheduled dose.
Ethanol therapy: Increase to 3.0 mL/kg/h at the time of hemodialysis and decrease to 1.5 mL/kg/h after hemodialysis; closely monitor serum ethanol and glucose level; adverse events include hypoglycemia, fluid overload, inebriation.
Continue 4MP/ethanol treatment until undetectable serum EG level (significant EG may rebound following hemodialysis).
Clinical-biochemical manifestation: Latent onset 8-12 h; variable with coingestion of ethanol.
Osmol and anion gap: An inverse relationship occurs with time; not a sensitive surrogate marker for toxic alcohol exposure.
Sodium bicarbonate: Large doses may be needed to treat metabolic acidosis; hypocalcemia.
4MP and ethanol only inhibit metabolism of toxic alcohols.
Isopropanol
Neurologic: CNS dysfunction/depression, coma.
Metabolic: Acetonemia, acetonuria, anion gap metabolic acidosis (mild).
CV: Hypotension, myocardial depression.
Supportive care
Maximize GFR: See Ethylene glycol.
Hemodialysis consideration: Hypotension (systolic <100 mm Hg), coma, or serum isopropanol ≥400 mg/dL (66.7 mmol/L).
Isopropanol is metabolized to acetone, and high serum acetone concentration can give falsely high serum Cr concentration with Jaffe-alkalinepicrate-colorimetric method used on automated chemistry instruments.
Methanol (MeOH)
Neurologic: CNS dysfunction/depression, coma.
Metabolic: Anion gap metabolic acidosis.
Ophthalmologic: Blindness.
Serum bicarbonate <20 mmol/L or arterial pH <7.30: See Ethylene glycol.
Known or high index of suspicion of ingestion, clinical poisoning, or serum MeOH level exceeding 20 mg/dL (6.3 mmol/L): IV 4MP or ethanol; See Ethylene glycol.
Maximize GFR: See Ethylene glycol.
IV leucovorin 2 mg/kg (infusion rate <160 mg/min) every 4-6 h until toxic alcohol is undetectable; clear clinical-biochemical recovery; if leucovorin not available IV folic acid 50-70 mg every 4 h; leucovorin preferred over folic acid.
Consider hemodialysis when CNS, visual, or funduscopic abnormality; serum MeOH ≥25 mg/dL (7.8 mmol/L); acidemia or renal insufficiency.
Leucovorin: Administer additional dose at end of hemodialysis.
Continue 4MP/ethanol treatment until undetectable serum MeOH level (significant MeOH may rebound following hemodialysis).
Clinical-biochemical manifestation, osmol and anion gap, sodium bicarbonate, 4MP/ethanol: See Ethylene glycol.
Hallucinations, agitated delirium: See Withdrawal syndrome, sedative hypnotics; IV diazepam or lorazepam, propofol or pentobarbital.
Physostigmine diagnostic aid: Selective use in anticholinergic agitation and delirium resulting from unknown ingestion; a positive response (e.g., patient awakens, provides history consistent with anticholinergic toxicity) obviates additional testing (e.g., cranial CT and lumbar puncture); IV physostigmine 0.5-2 mg at ≤0.5 mg/min (Peds: 0.02 mg/kg at 0.5 mg/min), if no reversal of anticholinergic effect within 10-20 min, administer an additional 1-2 mg.
Hyperthermia: Rapid cooling measures.
Urinary retention: Insert Foley catheter.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients followed by activated charcoal (oral/nasogastric) 1-2 g/kg.
Physostigmine: Contraindications include bronchospasm, mechanical intestinal or urogenital tract obstruction, early (<6 h) cyclic antidepressant overdose, overdose with cardiac conduction delay, and cyclic antidepressant poisoning with high-dose/drug-level phenomena (e.g., hypotension, coma, seizures, cardiac conduction delays, and dysrhythmias); complications include dehydration and rhabdomyolysis.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients; activated charcoal (oral/nasogastric) 1-2 g/kg followed by activated charcoal hourly, every 2 h, or every 4 h at a dose equivalent to 12.5 g/h (Peds: 10-25 g) for 12-24 h, not in patients with decreased bowel sounds/ileus; WBI (See Box 96-2) for large ingestion of modified release formulation; procedural removal of bezoar/concretion.
Extracorporeal elimination (i.e., hemodialysis, hemoperfusion, CVVH) consideration: Persistently high serum CBZ concentrations and coma.
Pharmacobezoar: Serum CBZ concentration continues to significantly rise or not significantly decreasing over time, delayed symptoms, relapse, or deteriorate after appropriate GI decontamination as late as 48 h after overdose; imaging studies with contrast to confirm diagnosis.
Risk stratification based on peak serum CBZ concentration:
Delayed peak concentration following modified released formulation may be >96 h.
CV: Dysrhythmias; hypotension; heart failure; respiratory arrest; asystole from propylene glycol toxicity during rapid IV phenytoin administration (e.g., >50 mg/min).
Activated charcoal (oral/nasogastric) 1-2 g/kg; administer additional activated charcoal hourly, every 2 h, or every 4 h at a dose equivalent to 12.5 g/h (Peds: 10-25 g) for 12-24 h in patients with serum phenytoin concentration >40 µg/mL, moderate neurologic toxicity, or rising serum phenytoin levels following initial activated charcoal dose, but not in patients with decreased bowel sounds/ileus; discontinue before drug levels reach therapeutic range in patients on phenytoin therapy.
Metabolic: Anion gap metabolic acidosis; hyperammonemia; hypernatremia; hypocalcemia.
Hematologic: Thrombocytopenia; leukopenia.
Coma, symptomatic hyperammonemia, symptomatic hepatotoxicity, or rising serum ammonia levels: IVL-carnitine 100 mg/kg (max 6 g) over 30 min followed by 15 mg/kg every 4 h over 10-30 min until clinical improvement; consider treatment for patients with serum VPA >450 µg/mL.
Acute VPA overdose without hepatic enzyme abnormalities or hyperammonemia: Consider oral L-carnitine 100 mg/kg/d (max 3 g) divided every 6 h.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients followed by activated charcoal (oral/nasogastric) 1-2 g/kg; WBI (See Box 96-2) for large ingestion of modified release formulation; procedural removal of bezoar/concretion.
Consider hemodialysis when coma, hemodynamic instability, rapid deterioration, hepatic dysfunction, metabolic acidosis unresponsive to fluids, serum VPA >1,000 µg/mL; terminate when serum VPA is in the therapeutic range.
Risk stratification based on peak serum VPA concentration:
Delayed peak concentration may be >10 h postingestion.
Hemodialysis and CAVH/CVVH are not equivalent, and they are not mutually exclusive; CAVH/CVVH may be the only option in hypotensive patients until hemodialysis can be tolerated.
ECG (maximal limb-lead) QRS ≥120 ms or RaVR ≥3 mm or R/SaVR ≥0.7: IV sodium bicarbonate 1-2 mmol/kg bolus × 2; repeat ECG every 3-5 min; IV sodium bicarbonate 1-2 mmol/kg bolus until the QRS duration stabilized.
Seizures and dysrhythmias: Current ACLS toxicology guidelines and avoid class IA/IC antidysrhythmics; class IB may be useful.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients, followed by activated charcoal (oral/nasogastric) 1-2 g/kg; WBI (See Box 96-2) for large ingestion of modified release formulation; procedural removal of bezoar/concretion.
Bupropion seizures: Therapeutic or overdose; brief; latent onset 10-24 h (sustainedrelease preparations).
Amoxapine seizures: Recurrent and prolonged.
Monoamine oxidase inhibitors (MAOI)
Latent-onset toxicity (6-24 h); sympathetic hyperactivity with CNS excitation and peripheral sympathetic stimulation (e.g., hypertension, tachycardia, tachypnea, pyrexia, agitation, confusion, tremor, hyperreflexia); may progress to CNS depression and CV collapse.
Sympathetic hyperactivity: IV BZD; neuromuscular paralysis and intubation; cooling measures.
Severe hypertension and tachycardia: IV nitroprusside and esmolol.
Hypotension: IV norepinephrine or epinephrine (avoid dopamine).
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): See Cyclic antidepressant.
Maximize GFR: IV NS target urine output 2-4 mL/kg/h.
MAOI: Combined with serotoninergic drugs is a significant risk for severe serotonin syndrome/death; interaction with sympathomimetics (e.g., amphetamines, ephedrine, phenylephrine) and tyramine in food (e.g., aged cheese, smoked/pickled meats, red wine, pasteurized light, pale beers) precipitate “hypertensive crisis” (i.e., agitation, tachycardia, hyperthermia, seizures) and ICH.
Serotonin syndrome (toxicity): Spontaneous clonus; inducible clonus and agitation or diaphoresis; ocular clonus and agitation or diaphoresis; tremor and hyperreflexia; hypertonic and temperature >38°C; and ocular or inducible clonus.
Neuroexcitation/serotonin syndrome: IV BZD; IV chlorpromazine 50 mg, repeat in 2-3 h as needed or oral (gastric tube) cyproheptadine 4-8 mg (max 24 mg/d), and repeat every 2 h if no improvement or recurrent signs; neuromuscular paralysis and intubation; cooling measures.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): See Cyclic antidepressant.
Maximize GFR: See MAOI.
Serotonin syndrome (toxicity): Can be caused by all antidepressants, alone or in combination, in therapeutic or overdoses, in combination with other serotonergic agents; escalating dose or additional serotonergic agent during chronic therapy; a spectrum of serotonin-related adverse events progressing to toxicity; complications include rhabdomyolysis, dysrhythmias.
Symptomatic/severe poisoning or known/suspected chloroquine ingestion >5 g:
Rapid orotracheal intubation and avoid thiopental induction.
AND
IV epinephrine 0.25 µg/kg/min followed by increments of 0.25 µg/kg/min until systolic arterial pressure ≥100 mm Hg).
AND
IV diazepam 2 mg/kg over 30 min followed by 1-2 mg/kg/d × 2-4 d.
Transient CV compromise requires additional epinephrine and other catecholamines.
Heart block or ECG (maximal limb-lead) QRS ≥120 ms: IV sodium bicarbonate 1-2 mmol/kg bolus × 2; repeat ECG every 3-5 min; IV sodium bicarbonate 1-2 mmol/kg bolus until QRS duration stabilized.
Seizures and dysrhythmias: Current ACLS toxicology guidelines and avoid class IA/IC/III antidysrhythmics; class IB may be useful.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients followed by activated charcoal (oral/nasogastric) 1-2 g/kg.
Acute chloroquine poisoning results in hypokalemia (intracellular shifts, not total body depletion) that reflects severity of toxicity; carefully monitor serum potassium concentrations, particularly among patients who also receive catecholamine infusions; overzealous potassium replacement invokes risk of subsequent hyperkalemia.
Quinine
Ophthalmologic: Blurred vision; visual field constriction, scotomata; diplopia; altered color perception; complete blindness (sudden visual loss can occur ≥14 h after overdose); pupils dilated and unreactive in proportion to the degree of visual impairment.
Neurologic: Delirium, coma, and seizures; tinnitus, deafness.
Metabolic: Hypoglycemia rare except during high-dose IV quinine and concomitant metabolic stresses (e.g., malaria, malnutrition, alcoholism).
Respiratory: ARDS.
Heart block or ECG (maximal limb-lead) QRS ≥120 ms (See Chloroquine).
Seizures and dysrhythmias: See Chloroquine.
Hypoglycemia: IV dextrose (monitor serum potassium and QTc) or IV octreotide 50 µg/h or IM octreotide 100 µg.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients; activated charcoal (oral/nasogastric) 1-2 g/kg followed by hourly, every 2 h, or every 4 h at a dose equivalent to 12.5 g/h (Peds: 10-25 g) for 12-24 h; not in patients with decreased bowel sounds/ileus.
Complete blindness reported only after oral quinine ingestion and expected (can be lower) when serum quinine >20 mg/mL in the first 10 h following ingestion; residual impairment (e.g., peripheral field defects, scotomata, impaired color vision, complete blindness) in severe cases.
Patients on therapeutic doses of quinine may experience nausea, vomiting, decreased hearing acuity, tinnitus, headache, and tachycardia (“cinchonism”).
Beta-adrenergic blocker (BB)
CV: Hypotension and bradycardia (pindolol-tachycardia and hypertension); heart failure, pulmonary edema; IVCD (e.g., acebutolol, betaxolol, carvedilol, metoprolol, oxprenolol, and propranolol); heart block; ventricular dysrhythmias; asystole.
Neurologic: Depressed consciousness; confusion; lethargy; coma; seizures (especially BB with high lipid solubility-propranolol, penbutolol, metoprolol).
Respiratory: Bronchospasm.
Metabolic: Hypoglycemia/hyperglycemia (rare).
Bradycardia:
IV atropine (max 3 mg).
IV glucagon 50-150 mg/kg and start infusion dose to give effective bolus dose each hour (e.g., heart rate increased after two successive 5-mg boluses, then administer 10 mg/h).
Cardiac pacing: Optimal pacing rate 50-60 beats per minute.
Hypotension: IV NS bolus, catecholamine(s).
QRS >120 ms: IV sodium bicarbonate 1-2 mmol/kg bolus; repeat for recurrent QRS widening.
Hypodynamic myocardium. Euglycemic clamp:IV regular insulin 1 IU/kg bolus followed by infusion 0.5 IU/kg/h titrated every 30 min to desired effect on contractility or blood pressure (echocardiography for measuring myocardial response); euglycemia = serum glucose 100-250 mg/dL (5.5-14 mmol/L) is maintained by IV dextrose 25 g bolus with initial insulin bolus (unless serum glucose >400 mg/dL [22 mmol/L]) followed by dextrose infusion 0.5 g/kg/h titrated based on bedside glucose monitoring every 20-30 min until serum glucose is stable and then every 1-2 h; replace potassium if <2.5 mmol/L and a source of potassium loss.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): Gastric lavage (See Box 96-1) in acutely sick patients followed by activated charcoal (oral/nasogastric) 1-2 g/kg; WBI (See Box 96-1) for large ingestion of modified release formulation; endoscopic removal of bezoar/concretion.
Bradycardia/hypotension seldom responds to atropine and fluid bolus.
Glucagon most effective in increasing heart rate.
Cardiac pacing: Often fails to capture; blood pressure not always restored.
Catecholamine use/dosing based on cardiodynamic and hemodynamic monitoring (e.g., norepinephrine for hypotension due to low SVR); no one catecholamine superior for CV drug toxicity and may require large doses of multiple adrenergic agents.
Euglycemic clamping: Response not immediate and increase chance of benefit with early detection of hypodynamic myocardium and early initiation of therapy; numerical hypoglycemia, hypokalemia, hypophosphatemia, hypomagnesemia.
Body packer
Asymptomatic: Presents in custody of law enforcement officer(s) requesting medical evaluation or retreival of contraband from the GI tract; medicolegal issues may be involved.
Symptomatic: Typical signs/symptoms of the drug (e.g., cocaine, heroin) being concealed.
May present with or develop signs/symptoms of intestinal obstruction, intestinal perforation, peritonitis.
Asymptomatic: Administer an oral dose of water-soluble contrast (e.g., Gastrografin) 1 mL/kg; perform abdominal radiographs (supine and upright) at least 5 h after contrast administration; perform daily abdominal radiographs if radiographs are positive and after a spontaneous bowel movement; check all bowel movements for drug packets; continue until after passage of two packet-free bowel movements and negative abdominal radiographs; oral intake ad lib.
Symptomatic heroin body packer: IV naloxone infusion (See Opioid); activated charcoal (oral/nasogastric) 1-2 g/kg, and WBI (See Box 96-2) after patient stablized, patient is able to tolerate charcoal/WBI, and precautionary measures to minimize aspiration.
Surgical intervention: Symptomatic cocaine body packer; failed medical management in symtomatic heroin body packer; intestinal obstruction/perforation; packets fail to progress through the GI tract after conservative management.
Consider endoscopic retrieval of retained packets in the stomach by an experienced endoscopist.
Calcium channel antagonist (CCA)
CV: See Beta-adrenergic blocker (BB); bepridilprolonged QTc and torsade de pointes.
Neurologic: See BB.
Metabolic: Hyperglycemia; lactic acidosis.
Respiratory: Noncardiogenic pulmonary edema.
Abdomen: Ileus; mesenteric ischemia/infarction.
Bradycardia: See BB.
Hypotension: See BB.
QRS >120 ms: See BB.
Hypodynamic myocardium
See BB.
IV calcium gluconate (10%) 0.6 mL/kg bolus (0.2 mL/kg 10% calcium chloride) over 5-10 min followed by continuous calcium gluconate infusion at 0.6-1.5 mL/kg/h (0.2-0.5 mL/kg/h 10% calcium chloride); titrate infusion to affect improved blood pressure/contractility; follow ionized calcium levels every 30 min initially and then every 2 h maintaining ionized calcium twice normal.
GI decontamination consideration (after patient stabilized and precautionary measures to minimize aspiration): See BB.
