Severe Tetanus dg Autonomic Storm

Severe tetanus is associated with profound autonomic instability.
This usually starts a few days after the spasms and lasts 1–2 weeks.
Increased sympathetic tone causes vasoconstriction, tachycardia and hypertension. 

‘Autonomic storms’ are associated with raised catecholamine levels. These alternate with episodes of :

• sudden hypotension
• sudden bradycardia 
• sudden asystole. 

Other features of autonomic disturbance include :

• salivation
• sweating
• increased bronchial secretions
• hyperpyrexia
• gastric stasis
• ileus

Ablett classification of tetanus severity

Grade 1 (mild)

Mild trismus, general spasticity, no respiratory compromise, no spasms, no dysphagia

Grade 2 (moderate)

Moderate trismus, rigidity, short spasms, mild dysphagia, moderate respiratory involvement, ventilatory frequency >30

Grade 3 (severe)

Severe trismus, generalized rigidity, prolonged spasms, severe dysphagia, apnoeic spells, pulse >120, ventilatory frequency >40

Grade 4 (very severe)

Grade 3 with severe autonomic instability

Management Principples

• Early intervention with airway (Tracheotomy and mechanical ventilatory support )
• Spasm control ( Neuromuscular blocking agents )
• Well sedated while paralyzed

Drugs :

1. The benzodiazepines are the most widely used agents currently available for the control of tetanic spasms and rigidity. Properties : Sedation and amnesia
2. A continuous infusion of midazolam in large doses could also be employed.  Using diazepam up to 35 mg (1 mg/kg/dose) every 3 hours (280 mg/day). 
3.  Morphine therapy to control autonomic hyperactivity. It has been given in doses of 1-2 mg/kg every 12 hours for 22 days 
4. Labetalol initially as intermittent IV boluses 0.25-1.0 mg/kg and was then placed on continuous infusion of 2 mg/kg/hr. The infusion was weaned over four days with no further episodes of hypertension.  Labetalol is both an alpha- and beta-adrenergic blocking agent. It also inhibits the uptake of norepinephrine into nerve terminals. It was used successfully in controlling the labile hypertension when the combination of heavy sedation, narcotic analgesia, and muscle paralysis failed. 
5. Clonidine, in combination with magnesium, sedation and paralysis, provided better control. The narrow margin between therapeutic toxic blood level of magnesium as well as the need for frequent monitoring of magnesium level may limit its use for this purpose.

The syndrome of sympathetic nervous hyperactivity :

1. sustained but labile hypertension and tachycardia
2. irregularities of cardiac rhythm, 
3. peripheral vascular constriction
4. profuse sweating, pyrexia
5. increased carbon dioxide output
6. increased catecholamine excretion

Prolonged sympathetic overactivity may end with profound and preterminal hypotension and bradycardia; it often indicates imminent death. Parasympathetic overactivity may lead to preterminal bradycardia and sinus arrest, salivation and increased bronchial secretions. Direct damage to the vagal nucleus has been implicated, as well as local damage to the sinus node, and to reflex excessive vagal tone.