What are the causes of muscle rigidity in a moribund patient?

Causes of Muscle Rigidity in a Moribund Patient

In a moribund patient, muscle rigidity most commonly results from neuroleptic malignant syndrome (NMS), malignant hyperthermia, tetanus, severe sepsis with metabolic derangements, or drug-induced hypermetabolic states—all life-threatening conditions requiring immediate recognition and intervention.

Life-Threatening Drug-Induced Causes

Neuroleptic Malignant Syndrome (NMS)

• NMS presents as a tetrad of mental status changes, fever, hypertonicity/rigidity, and autonomic dysfunction due to dopamine D2 receptor blockade in the CNS 1
• The pathophysiology involves D2 receptor antagonism in nigrostriatal pathways and spinal cord producing muscle rigidity, while peripheral calcium release from sarcoplasmic reticulum causes increased contractility, heat production, and muscle breakdown 1
• Mortality has decreased from 76% in the 1960s to <10-15% currently, but remains lethal without prompt recognition 1
• Risk factors include coadministration of multiple psychotropic agents (>50% of cases), dehydration, physical exhaustion, and preexisting organic brain disease 1
• Consider NMS in any moribund patient with fever and altered mental status who is taking or may have taken an antipsychotic medication 1

Malignant Hyperthermia

• Characterized by fulminant hypermetabolism of skeletal muscle with skeletal muscle rigidity, tachycardia, tachypnea, hypercarbia, metabolic acidosis, and fever 2
• Triggered by inhalation anesthetics or depolarizing muscle relaxants in susceptible individuals 2, 3
• Dantrolene sodium is the specific treatment and should be administered by continuous rapid IV push as soon as recognized 2
• The hypermetabolic reaction leads to rapidly evolving rigidity, extensive rhabdomyolysis, and hyperkalemia 3

Serotonin Syndrome

• Results from excessive serotonergic activity, presenting with hyperthermia, muscle rigidity, and altered mental status 3
• Frequently accompanied by intense skeletal muscle hypermetabolic reaction leading to rhabdomyolysis and hyperkalemia 3

Infectious Causes

Tetanus

• Produces severe muscle rigidity and spasms due to tetanospasmin blocking inhibitory neurotransmitters 1, 3
• Hypoxemia and metabolic acidosis are common at admission and predict mortality 4
• Mortality is significantly higher in patients with admission PaO2 <70 mmHg (p<0.01) or pH <7.2 (p<0.05) 4
• Muscle relaxants may be needed to control severe muscle spasms, though succinylcholine should be avoided in immobilized patients 1

CNS Infections

• Encephalitis and meningitis can present with rigidity, altered mental status, and fever 3
• Must be differentiated from drug-induced causes through CSF analysis and imaging 3

Metabolic and Systemic Causes

Severe Sepsis with Metabolic Derangements

• Muscle relaxants should NOT be used in sepsis except for endotracheal intubation and mechanically ventilated patients with severe respiratory distress 1
• Metabolic acidosis from tissue hypoperfusion can contribute to muscle dysfunction 1
• Prolonged immobilization (≥3 days) creates risk for hyperkalemia if depolarizing muscle relaxants are used 1

Rhabdomyolysis and Myonecrosis

• Excessive calcium accumulation in skeletal muscle causes myocyte death and severe muscle rigidity 1
• Can result from drug-induced hypermetabolic states, prolonged immobilization, or severe metabolic derangements 1
• Monitor creatine kinase and potassium closely to prevent myoglobinuric renal failure and dysrhythmias 1

Neurological Causes in Moribund Patients

Progressive Encephalomyelitis with Rigidity and Myoclonus (PERM)

• Rare subacute disorder characterized by muscle rigidity, stimulus-sensitive spasms, and brainstem dysfunction with poor prognosis 1
• Associated with glycine receptor antibodies (GlyR-Abs) in some cases 1
• Pathological findings include perivascular lymphocyte cuffing and neuronal loss in brainstem and spinal cord 1

Parkinsonism (Less Likely in Acute Moribund State)

• Rigidity presents as constant resistance to passive movement throughout entire range of motion 5, 6
• Typically develops gradually after 40-50% of dopaminergic neurons are lost, not acutely in moribund patients 5
• Lead-pipe rigidity shows smooth constant resistance; cogwheel rigidity has ratchet-like quality when combined with tremor 5

Critical Diagnostic Algorithm

Step 1: Medication History

• Identify any antipsychotic use (typical or atypical), recent anesthesia exposure, or serotonergic agents 1, 3
• Check for recent changes in psychotropic medications or dopamine agonist withdrawal 1

Step 2: Vital Signs and Associated Features

• Fever + rigidity + altered mental status + autonomic instability = NMS until proven otherwise 1
• Tachycardia, tachypnea, hypercarbia, and metabolic acidosis suggest malignant hyperthermia 2
• Stimulus-sensitive spasms with preserved consciousness suggest tetanus 4, 3

Step 3: Laboratory Evaluation

• Creatine kinase (markedly elevated in NMS, malignant hyperthermia, rhabdomyolysis) 1, 3
• Arterial blood gas (hypoxemia and acidosis predict mortality in tetanus) 4
• Electrolytes, particularly potassium (hyperkalemia from muscle breakdown) 1, 3
• Blood cultures and inflammatory markers if sepsis suspected 1

Step 4: Immediate Management Priorities

• Discontinue all potential causative agents immediately 1, 3
• Aggressive temperature reduction for drug-induced hyperthermia 3
• Dantrolene sodium for confirmed or suspected malignant hyperthermia 2
• Supportive care in intensive care setting with close monitoring 1, 3

Critical Pitfalls to Avoid

• Do NOT use succinylcholine in patients immobilized ≥3 days or with neuromuscular diseases due to risk of treatment-resistant hyperkalemia 1
• Do NOT use muscle relaxants in septic patients except for intubation or severe respiratory distress 1
• Do NOT delay treatment while awaiting confirmatory tests in suspected NMS or malignant hyperthermia—these are clinical diagnoses requiring immediate intervention 1, 2, 3
• Do NOT confuse parkinsonian rigidity (chronic, progressive) with acute rigidity in moribund patients 5, 6
• Do NOT assume rigidity is solely neurological—always consider metabolic, infectious, and drug-induced causes first in acute presentations 3