Essential Drugs in Casualty: A Clinically Verified Pharmacological Overview

 Essential Drugs in Casualty: A Clinically Verified Pharmacological Overview

Author: Dr. Shekhar and team Doctor's forum for all 🏥 

Disclaimer: The following article is intended strictly for educational purposes and should not be used as a substitute for professional medical judgment, diagnosis, or treatment. Clinical decisions must be based on individual patient assessment, local protocols, and the most current evidence-based guidelines.

Introduction

The casualty (emergency) department demands rapid, decisive pharmacological intervention across a spectrum of life-threatening conditions. Drugs used here must possess predictable pharmacokinetics, rapid onset, high therapeutic indices, and familiarity among frontline clinicians. This article provides an exhaustive review of emergency medications categorized by system and clinical scenario, detailing pharmacology, mechanism of action, and the pathological conditions they address. All information is synthesized from established critical care, cardiology, and emergency medicine literature, as referenced at the end of the document.

1. Cardiovascular Emergencies

1.1 Cardiac Arrest and Peri-Arrest Arrhythmias

Adrenaline (Epinephrine)

· Pharmacology: Endogenous catecholamine with potent α- and β-adrenergic agonism. In cardiac arrest, 1 mg (10 mL of 1:10,000 solution) IV/IO every 3–5 minutes. Onset is immediate; duration 5–10 minutes. Metabolized by MAO and COMT (1,2).

· Mechanism of Action: α₁-mediated vasoconstriction raises systemic vascular resistance, increasing coronary and cerebral perfusion pressure during CPR. β₁-receptor stimulation enhances myocardial contractility and heart rate, raising myocardial oxygen demand; this is beneficial during arrest but theoretically deleterious post-ROSC. β₂ effects cause bronchodilation and stabilize mast cells (useful in anaphylaxis) (1,3).

· Pathological Conditions: Cardiac arrest (VF/VT, asystole, PEA), anaphylactic shock, severe croup, bradycardia unresponsive to atropine (4).

Amiodarone

· Pharmacology: Class III antiarrhythmic (Vaughan Williams) with additional Class I, II, and IV properties. IV formulation contains polysorbate 80 and benzyl alcohol, risking hypotension and phlebitis. Highly lipophilic, large volume of distribution, hepatic metabolism via CYP3A4 to desethylamiodarone. Elimination half-life 20–100 days (2,5).

· Mechanism of Action: Prolongs cardiac action potential duration (phase 3) by blocking potassium channels, thus lengthening refractory period in atria, ventricles, AV node, and accessory pathways. Additional sodium channel blockade (Class I), non-competitive β-blockade (Class II), and calcium channel blockade (Class IV) contribute to antiarrhythmic efficacy (2,6).

· Pathological Conditions: Shock-refractory ventricular fibrillation/pulseless ventricular tachycardia (after third shock, 300 mg IV bolus, then 150 mg). Stable ventricular tachycardia, atrial fibrillation with rapid ventricular response in Wolff-Parkinson-White syndrome, supraventricular tachycardias (4,7).

Lidocaine

· Pharmacology: Class IB antiarrhythmic, amide-type local anesthetic. IV dose 1–1.5 mg/kg bolus, followed by 0.5–0.75 mg/kg repeat doses up to 3 mg/kg. Hepatic metabolism (CYP3A4, CYP1A2), half-life ~2 hours in normal hepatic function (2,5).

· Mechanism of Action: Blocks fast sodium channels preferentially in ischemic or depolarized tissue, slowing phase 0 depolarization, reducing automaticity, and shortening action potential duration in Purkinje fibers. Elevates ventricular fibrillation threshold (6).

· Pathological Conditions: Alternative to amiodarone in cardiac arrest (VF/pulseless VT) when amiodarone unavailable. Stable ventricular tachycardia, prevention of post-cardioversion arrhythmias. Also used for digitalis-toxic arrhythmias (though magnesium preferred) (4,7).

Atropine

· Pharmacology: Tertiary amine alkaloid, anticholinergic. IV dose 0.5–1 mg every 3–5 minutes (max 3 mg) for bradycardia. Onset 1–2 minutes; duration 2–6 hours. Crosses blood-brain barrier (1,2).

· Mechanism of Action: Competitive antagonist at peripheral and central muscarinic (M₂, M₃) acetylcholine receptors. In the heart, M₂ blockade increases sinoatrial node firing rate and AV conduction velocity by reducing vagal tone. Also inhibits secretions and causes pupillary dilation (1).

· Pathological Conditions: Symptomatic sinus bradycardia, AV block (second-degree type I), organophosphate poisoning (high-dose 2–5 mg IV), premedication for rapid sequence intubation (to prevent bradycardia in children <1 year) (4,8).

Adenosine

· Pharmacology: Endogenous purine nucleoside. IV bolus 6 mg → 12 mg → 12 mg via rapid proximal IV push followed by saline flush. Half-life <10 seconds; metabolized by endothelial cells and erythrocytes via adenosine deaminase (2,5).

· Mechanism of Action: Activates A₁ adenosine receptors on atrial and AV nodal myocytes, opening G-protein-coupled potassium channels (K_Ach), causing hyperpolarization and transient conduction block. This terminates re-entrant supraventricular tachycardias involving the AV node. Also coronary vasodilator (used in stress testing) (6).

· Pathological Conditions: Paroxysmal supraventricular tachycardia (AVRT, AVNRT). Diagnostic aid in wide-complex tachycardia of uncertain origin. Also used for pharmacological stress testing (4,7).

Calcium Chloride / Gluconate

· Pharmacology: Calcium salt solutions: calcium chloride 10% (100 mg/mL, 1.36 mEq Ca²⁺/mL) or calcium gluconate 10% (100 mg/mL, 0.465 mEq Ca²⁺/mL). Rapid IV push. Calcium chloride preferred in emergencies due to higher bioavailability of ionized calcium (1,5).

· Mechanism of Action: Essential cation for myocardial excitation-contraction coupling, smooth muscle contraction, and neurotransmitter release. Antagonizes the cardiotoxic effects of hyperkalemia by stabilizing myocardial membrane potential (3,9).

· Pathological Conditions: Hyperkalemia with ECG changes, calcium channel blocker overdose (high-dose IV calcium), hypocalcemia (tetany, prolonged QT), fluoride toxicity, magnesium sulfate overdose (4,8).

2. Respiratory Emergencies

2.1 Bronchospasm and Anaphylaxis

Salbutamol (Albuterol)

· Pharmacology: Short-acting β₂-adrenergic agonist. Nebulized (2.5–5 mg) or metered-dose inhaler (90–180 µg). Onset 5–10 minutes; duration 4–6 hours (2,5).

· Mechanism of Action: Selectively stimulates β₂-receptors on bronchial smooth muscle, activating adenylate cyclase → ↑cAMP → relaxation. Also inhibits mast cell mediator release and enhances mucociliary clearance (1).

· Pathological Conditions: Acute asthma exacerbation, COPD exacerbation, hyperkalemia (shifts potassium intracellularly via β₂-agonism), anaphylaxis (adjunctive) (4,8).

Ipratropium Bromide

· Pharmacology: Quaternary ammonium anticholinergic. Nebulized 0.5 mg combined with salbutamol. Poorly absorbed systemically; minimal CNS effects (2,5).

· Mechanism of Action: Blocks M₃ muscarinic receptors on bronchial smooth muscle, reducing vagally mediated bronchoconstriction. Also decreases submucosal gland secretion (1).

· Pathological Conditions: Severe acute asthma, COPD exacerbation (often in combination with β₂-agonists) (4,7).

Adrenaline (Intramuscular)

· Pharmacology: As above; IM dose 0.3–0.5 mg (1:1,000 solution) into anterolateral thigh. Rapid absorption, peak ~5–10 minutes (2).

· Mechanism of Action: α₁ agonism reduces airway edema and urticaria; β₂ agonism causes bronchodilation; β₁ increases cardiac output, supporting perfusion. Stabilizes mast cells, preventing further histamine release (1,3).

· Pathological Conditions: Anaphylaxis (first-line), severe croup, acute angioedema (4,8).

Hydrocortisone / Methylprednisolone

· Pharmacology: Glucocorticoids. IV hydrocortisone 200 mg, methylprednisolone 125 mg. Onset of genomic effects 4–6 hours; rapid non-genomic effects may exist (2).

· Mechanism of Action: Bind glucocorticoid receptor, translocate to nucleus, and modulate gene transcription: upregulate anti-inflammatory mediators (lipocortin-1) and downregulate pro-inflammatory cytokines (IL-1, TNF-α, COX-2). Reduce airway mucosal edema, eosinophil recruitment, and mucus secretion (1,10).

· Pathological Conditions: Acute severe asthma, anaphylaxis (adjunctive to prevent biphasic reactions), COPD exacerbation, croup, spinal cord injury (high-dose methylprednisolone within 8 hours) (4,8).

3. Neurological Emergencies

3.1 Status Epilepticus

Lorazepam / Midazolam / Diazepam

· Pharmacology: Benzodiazepines. Lorazepam IV 4 mg (repeat once), midazolam IM/IV 10 mg, diazepam IV 5–10 mg (rectal 0.5 mg/kg for children). Lorazepam less lipid-soluble, slower brain redistribution, longer anticonvulsant effect (2,5).

· Mechanism of Action: Bind to the benzodiazepine site on GABAₐ receptor, increasing frequency of chloride channel opening, enhancing GABA-mediated inhibition, raising seizure threshold (6).

· Pathological Conditions: Status epilepticus (first-line), acute seizures, alcohol withdrawal seizures, acute anxiety, procedural sedation (4,7).

Phenytoin / Fosphenytoin

· Pharmacology: Fosphenytoin is a water-soluble prodrug of phenytoin; administered IV in PE (phenytoin equivalents) 20 mg/kg, max rate 150 mg/min PE. Phenytoin saturable kinetics (zero-order at therapeutic range), CYP2C9/19 metabolism, highly protein-bound (2).

· Mechanism of Action: Stabilizes neuronal membrane by prolonging inactivated state of voltage-gated sodium channels in a use-dependent manner, limiting high-frequency repetitive firing without affecting normal neurotransmission (6).

· Pathological Conditions: Status epilepticus after benzodiazepines, prophylaxis in traumatic brain injury, acute seizures (4,8).

Levetiracetam

· Pharmacology: Broad-spectrum antiepileptic. IV dose 20–60 mg/kg (max 4.5 g). Renal excretion largely unchanged, minimal drug interactions, linear kinetics (2,5).

· Mechanism of Action: Binds synaptic vesicle protein SV2A, modulating neurotransmitter release. Also affects calcium homeostasis and GABA-ergic transmission (6).

· Pathological Conditions: Status epilepticus (alternative to phenytoin), acute seizures in neurosurgical patients, seizures in pregnancy (safest option) (4,7).

3.2 Acute Ischemic Stroke

Alteplase (tPA)

· Pharmacology: Recombinant tissue plasminogen activator. IV 0.9 mg/kg (max 90 mg), 10% bolus, remainder infused over 1 hour. Short half-life ~5 minutes; hepatic clearance (2).

· Mechanism of Action: Serine protease that converts plasminogen to plasmin, which degrades fibrin clots. Fibrin-specificity arises from increased activity when bound to fibrin (1,3).

· Pathological Conditions: Acute ischemic stroke within 3–4.5 hours of onset (according to guidelines), massive pulmonary embolism with hemodynamic instability, acute myocardial infarction when PCI not immediately available (4,8).

4. Metabolic and Toxicological Emergencies

Dextrose 50% (D50)

· Pharmacology: Hypertonic glucose solution, 25 g in 50 mL (D50W). Administered IV push (adults) for hypoglycemia. Rapidly distributed, metabolized to CO₂ and H₂O (5).

· Mechanism of Action: Provides immediate substrate for cerebral glucose metabolism, reversing neuroglycopenic symptoms (3).

· Pathological Conditions: Documented or suspected severe hypoglycemia (altered mental status, coma, seizures). Often given after thiamine to prevent Wernicke encephalopathy in malnourished patients (4,7).

Naloxone

· Pharmacology: Opioid receptor antagonist. IV/IM/IN dose 0.4–2 mg, repeated up to 10 mg. Onset <2 min IV. Duration 30–90 min, shorter than most opioids. Hepatic metabolism (2,5).

· Mechanism of Action: Competitive antagonist at μ, κ, and δ opioid receptors, with highest affinity for μ. Reverses respiratory depression, sedation, and miosis (1).

· Pathological Conditions: Known or suspected opioid overdose, respiratory depression from opioids, pruritus due to opioid-induced histamine release (4,8).

Flumazenil

· Pharmacology: Imidazobenzodiazepine, competitive antagonist at benzodiazepine binding site on GABAₐ receptor. IV 0.2 mg over 15 sec, repeated up to 1 mg. Short half-life 40–80 min; hepatic metabolism (2,5).

· Mechanism of Action: Displaces benzodiazepines from receptor, reversing sedation and respiratory depression. Does not reverse effects of other GABA-ergic agents (e.g., barbiturates, ethanol) (6).

· Pathological Conditions: Benzodiazepine overdose with respiratory depression, reversal of procedural sedation. Contraindicated in chronic benzodiazepine dependence (seizure risk), mixed overdose with tricyclic antidepressants (seizures), and undiagnosed seizure disorders (4,7).

Sodium Bicarbonate

· Pharmacology: Hypertonic 8.4% solution (1 mEq/mL). IV bolus 1–2 mEq/kg. Alkalinizing, generating CO₂ (5).

· Mechanism of Action: Buffers hydrogen ions via bicarbonate-carbonic acid system. Also provides sodium load which antagonizes cardiotoxic effects of hyperkalemia (membrane stabilization) and sodium channel blocker overdose (e.g., tricyclics) by overcoming channel blockade (3,9).

· Pathological Conditions: Severe metabolic acidosis (pH <7.1, cardiac dysfunction), hyperkalemia with ECG changes, sodium channel blocker poisoning (TCA overdose with QRS >100 ms), salicylate poisoning (urine alkalinization), crush syndrome (4,8).

N-Acetylcysteine (NAC)

· Pharmacology: Acetylated cysteine precursor. IV protocol: 150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours. Or oral 140 mg/kg loading, then 70 mg/kg q4h × 17 doses (2).

· Mechanism of Action: Replenishes hepatic glutathione stores, enabling detoxification of toxic paracetamol metabolite NAPQI. Also acts as a glutathione substitute and free radical scavenger, beneficial in hepatorenal protection (3,10).

· Pathological Conditions: Paracetamol (acetaminophen) overdose (time-sensitive, ideally within 8 hours; still indicated with delayed presentation). Also used for contrast-induced nephropathy prophylaxis (conflicting evidence) (4,8).

5. Sedation and Rapid Sequence Intubation (RSI)

Etomidate

· Pharmacology: Imidazole-derived anesthetic. Induction dose 0.3 mg/kg IV. Onset ~30 sec, duration 3–5 min. Hepatic ester hydrolysis. Minimal cardiovascular depression (5).

· Mechanism of Action: Enhances GABAₐ receptor activity, producing hypnosis. Less suppression of sympathetic outflow and cortisol synthesis (via 11β-hydroxylase inhibition) (6).

· Pathological Conditions: Induction agent for RSI in hemodynamically unstable patients (shock, trauma). No analgesic properties; combine with opioid. Adrenal suppression limit use in sepsis (controversial) (4,7).

Ketamine

· Pharmacology: Phencyclidine derivative. IV 1–2 mg/kg, IM 4–5 mg/kg. Hepatic metabolism (CYP2B6, 3A4) to norketamine (active). Dissociative anesthesia with analgesia (2).

· Mechanism of Action: Non-competitive NMDA receptor antagonist, blocking glutamate-mediated excitatory neurotransmission. Also interacts with opioid receptors (μ, κ) and monoamine transporters. Sympathomimetic effect: increases heart rate, blood pressure, bronchodilation (1,6).

· Pathological Conditions: RSI in hypotensive/trauma patients, severe asthma (bronchodilator effect), procedural sedation (especially in pediatrics), acute agitation combative patient, pain management (subdissociative doses) (4,8).

Succinylcholine

· Pharmacology: Depolarizing neuromuscular blocker. Dose 1–1.5 mg/kg IV. Ultrarapid onset (<60 sec), duration 5–10 min. Hydrolyzed by plasma pseudocholinesterase (2,5).

· Mechanism of Action: Mimics acetylcholine at nicotinic receptor (motor endplate), causing initial fasciculations followed by persistent depolarization and desensitization block, leading to flaccid paralysis (1).

· Pathological Conditions: RSI when rapid paralysis needed. Contraindications: hyperkalemia, burns >24h old, denervation injuries, muscular dystrophies, malignant hyperthermia susceptibility (4,7).

Rocuronium

· Pharmacology: Non-depolarizing aminosteroid neuromuscular blocker. Dose 1.2 mg/kg for RSI (high-dose, onset ~60 sec), maintenance 0.6 mg/kg. Duration ~40–60 min. Hepatic/renal elimination. Reversal with sugammadex (2).

· Mechanism of Action: Competitively binds to nicotinic cholinergic receptor at motor endplate, preventing acetylcholine-induced depolarization and muscle contraction (6).

· Pathological Conditions: RSI when succinylcholine contraindicated, maintenance of neuromuscular blockade during prolonged mechanical ventilation (4,8).

6. Volume Expansion and Vasoactive Agents

Crystalloids (Normal Saline, Ringer’s Lactate)

· Pharmacology: Isotonic electrolyte solutions. Bolus 250–1000 mL; rapid infusion. Distribution mainly in extracellular space; balanced solutions avoid hyperchloremic metabolic acidosis (3,9).

· Mechanism of Action: Expand intravascular volume by increasing hydrostatic pressure, improving preload and cardiac output. Ringer’s lactate contains bicarbonate precursor (lactate) to buffer acidosis (3).

· Pathological Conditions: Hypovolemic shock, distributive shock (sepsis, anaphylaxis), maintenance of hydration, fluid challenge (4,7).

Noradrenaline (Norepinephrine)

· Pharmacology: Endogenous catecholamine, predominantly α-agonist with some β₁ activity. IV infusion 0.05–3 mcg/kg/min titrated. Half-life ~2.5 min. Oxidized by MAO/COMT (2,5).

· Mechanism of Action: α₁-mediated vasoconstriction increases SVR, raising mean arterial pressure. β₁ effect increases cardiac contractility, modestly increases heart rate. Increases afterload, but in shock improves coronary perfusion (1,3).

· Pathological Conditions: Septic shock (first-line vasopressor), cardiogenic shock with low SVR, anaphylactic shock unresponsive to adrenaline, post-cardiac arrest hypotension (4,8).

Dobutamine

· Pharmacology: Synthetic catecholamine, racemic mixture. Infusion 2–20 mcg/kg/min. Onset 1–2 min; t½ ~2 min (2).

· Mechanism of Action: Predominantly β₁-adrenoceptor agonist, increasing myocardial contractility and heart rate. (-) isomer is α₁ agonist, (+) isomer is β₂ agonist and α₁ antagonist. Net effect: increased cardiac output, decreased SVR (afterload reduction), improved tissue perfusion (6).

· Pathological Conditions: Cardiogenic shock with low cardiac output and adequate SVR, septic cardiomyopathy when cardiac index is low, stress echocardiography (4,7).

7. Electrolyte Emergencies

Magnesium Sulfate

· Pharmacology: IV 2–4 g over 5–20 min for emergencies. Renal excretion. Therapeutic levels 1.5–2.5 mEq/L (2).

· Mechanism of Action: Cofactor for ATP-dependent enzymes. Blocks NMDA receptors (anticonvulsant), slows AV nodal conduction (treats torsades de pointes). Competitive calcium channel blocker, smooth muscle relaxant (tocolytic at high doses) (1,6).

· Pathological Conditions: Torsades de pointes/polymorphic VT, refractory VF (after lidocaine/amiodarone), severe asthma (nebulized or IV), eclampsia/pre-eclampsia (first-line seizure prophylaxis), hypomagnesemia (4,8).

Insulin (Regular) with Dextrose

· Pharmacology: Short-acting insulin IV push 10 units, often with 25 g dextrose (D50). Onset immediate; duration ~1 hour (2).

· Mechanism of Action: Binds insulin receptor, activating Na⁺/K⁺-ATPase pump, shifting potassium intracellularly. This temporarily lowers serum potassium independent of glycemic effect. Dextrose prevents hypoglycemia (3,9).

· Pathological Conditions: Severe hyperkalemia with ECG changes (emergent therapy, along with calcium, bicarbonate, β-agonists, dialysis). Also used in calcium channel blocker/β-blocker overdose with cardiogenic shock (high-dose insulin euglycemia therapy) (4,7).

8. Gastrointestinal Emergencies

Ondansetron

· Pharmacology: Serotonin 5-HT₃ receptor antagonist. IV/ODT 4–8 mg. Hepatic metabolism (CYP2D6, 3A4). QTc prolongation possible at high doses (2,5).

· Mechanism of Action: Blocks 5-HT₃ receptors in the chemoreceptor trigger zone and on vagal afferents in the GI tract, reducing nausea and vomiting signals to the vomiting center (1).

· Pathological Conditions: Acute nausea and vomiting  (gastroenteritis, chemotherapy, postoperative), prophylaxis for pediatric rehydration, motion sickness (off-label) (4,8).

9. Antidotes (Selected)

In addition to the agents already described, several specific antidotes are indispensable in the casualty department, each tailored to a particular intoxication.

Naloxone (opioid overdose) acts as a competitive antagonist at μ-opioid receptors, reversing respiratory depression and sedation at doses of 0.4–2 mg IV/IM/IN, repeated as needed up to 10 mg (4,7). Flumazenil (benzodiazepine overdose) displaces benzodiazepines from the GABAₐ receptor; it is given as 0.2 mg IV increments up to 1 mg, but must be avoided in chronic dependence, mixed tricyclic overdose, and seizure-prone patients due to the risk of refractory seizures (4,7). N-Acetylcysteine (paracetamol/acetaminophen poisoning) repletes hepatic glutathione, enabling safe conjugation of the toxic metabolite NAPQI; the standard IV regimen is 150 mg/kg over 1 hour, followed by 50 mg/kg over 4 hours and 100 mg/kg over 16 hours, with oral alternatives available (8,9).

Sodium bicarbonate (1–2 mEq/kg IV) serves as both buffer and sodium load in tricyclic antidepressant overdose, other sodium-channel blocker poisonings, and salicylate toxicity, while also being a critical temporizing measure in hyperkalemia (4,8). Calcium gluconate or calcium chloride (1–3 g IV) directly antagonizes the cardiotoxicity of hyperkalemia and stabilizes membranes in calcium channel blocker overdose and fluoride poisoning (9). Glucagon (5–10 mg IV) bypasses the blocked β-adrenergic receptor, activating adenylate cyclase directly, and is employed in severe beta-blocker and calcium channel blocker overdose when catecholamines fail (4,7).

Digoxin immune Fab (2–10 vials) binds free digoxin, rapidly reversing life-threatening digitalis toxicity including hyperkalemia and malignant arrhythmias (8). Hydroxocobalamin (5 g IV over 15 minutes) is the first-line antidote for cyanide poisoning, binding cyanide to form non-toxic cyanocobalamin, and is also indicated in smoke inhalation victims with altered mental status and lactic acidosis (4,8). Pralidoxime (2-PAM) (1–2 g IV bolus followed by infusion) reactivates organophosphate-inhibited acetylcholinesterase, complementing the muscarinic blockade of atropine in organophosphate poisoning (7,8). 20% Lipid emulsion (1.5 mL/kg bolus, then 0.25 mL/kg/min infusion) serves as a “lipid sink,” sequestering lipophilic local anesthetics and other cardiotoxic drugs in local anesthetic systemic toxicity (LAST), and has been used as rescue therapy in refractory cardiovascular collapse from lipophilic drug overdose (4,9).

(Sources: 4, 7, 8, 9)

Conclusion

Effective emergency pharmacotherapy demands an integrated understanding of a drug’s receptor interactions, pharmacokinetic profile, and the pathophysiological substrate of the condition being treated. The agents described above represent the core armamentarium of the casualty department, each validated by decades of clinical research and experience. Mastery of their pharmacology enables the clinician to navigate the chaos of emergencies with precision, titrating therapy against dynamic physiological derangements while anticipating adverse effects and drug interactions. Continuous reference to evolving international guidelines and institutional protocols remains essential for optimal patient outcomes.

References

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4. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142(16_suppl_2):S366-S468. doi:10.1161/CIR.0000000000000916

5. AHFS Drug Information® 2023. Bethesda, MD: American Society of Health-System Pharmacists; 2023.

6. Rang HP, Dale MM, Ritter JM, Flower RJ, Henderson G. Rang & Dale’s Pharmacology. 9th ed. Elsevier; 2020.

7. Tintinalli JE, Ma OJ, Yealy DM, et al., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill; 2020.

8. Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2023.

9. Marino PL. Marino’s The ICU Book. 5th ed. Wolters Kluwer; 2024.

10. Proudman RGW, Barnes PJ. Glucocorticoids. In: Clinical Respiratory Medicine. 4th ed. Elsevier; 2012:205-218.

This article is intended for educational purposes only and does not replace professional clinical judgment. Drug doses should be verified with current guidelines and local protocols. The author and publisher disclaim any liability for adverse effects resulting from use of this information.