Tick paralysis symptoms
anorexia, lethargy, muscle weakness, nystagmus, ascending flaccid paralysis
Ticks primarily responsible for tick paralysis
The ticks primarily responsible include :
Rocky Mountain wood tick (Dermacentor andersoni),
American dog tick (D. variabilis),
Lone Star tick (Amblyomma americanum),
black-legged tick (Ixodes scapularis),
western black-legged tick (I. pacificus),
Gulf coast tick (A. maculatum),
Australian Ixodes holocyclus.
Tick paralysis symptom onset
3-7 days after attachment of the tick
Tick paralysis patomech.
Several tick species produce a toxin that inhibits transduction at the neuromuscular junction by blocking influx of sodium ions. This prevents presynaptic terminal axon depolarization and inhibits release of acetylcholine at the nerve terminal. The toxin has not been fully identified.
The dominant clinical features of acute cholinergic toxicity include…
bradycardia, miosis, lacrimation, salivation, bronchorrhea, bronchospasm, urination, emesis, and diarrhea.
/symptoms of organophosphate and carbamate poisoning include typical muscarinic signs (lacrimation, bradycardia, bronchospasm) and nicotinic signs (mydriasis, tachycardia, weakness, hypertension). These result from the accumulation of acetylcholine in sympathetic ganglia and at the adrenal medulla. Increased depolarization at nicotinic neuromuscular synapses results in muscle weakness and flaccid paralysis. Central nervous system symptoms may be present, with suppression of central medullary centers resulting in anxiety, confusion, seizures, and coma./
Intermediate syndrome after organophosphorous agent poisoning
- 24-96 hrs
- 10-40 %
- cranial nerve abnormalities, neck flexion and proximal muscle weakness, respiratory insufficiency, and decreased deep tendon reflexes
Treatment of prganophosphate/carbamate poisoning
- endotracheal intubation and volume resuscitation is often needed
- aggressive decontamination with complete removal of the patient’s clothes and vigorous irrigation of the affected areas.
- Atropine is used for symptomatic relief of muscarinic symptoms. It does not reverse the paralysis caused by neuromuscular blockade that results from nicotinic receptor stimulation. Atropine dosing should be titrated to the therapeutic end point of the clearing of respiratory secretions and the cessation of bronchoconstriction.
- Pralidoxime and other oximes are effective in treating both muscarinic and nicotinic symptoms. Pralidoxime should not be administered without concurrent atropine, which prevents worsening symptoms due to transient oxime-induced acetylcholinesterase inhibition. Oxime therapy should be given to all patients with evidence of cholinergic toxicity, neuromuscular dysfunction, or exposure to organophosphorus agents known to cause delayed neurotoxicity.
Na channel blocker toxicity on the ECG
Tall R wave in aVR Tall R in V1 (sometimes) Tachycardia (usually) Right Axis Deviation Prolonged QRS
TCA overdose pearls
- Consider in patients with tachys and seizures
- ECG: RAD, tachycardia, wide QRS, tall R in aVR
- may be really wide complex tachycardia
- treat with sodium bicarb, consider lipid emulsion therapy
- normal antiarrhythmics will kill!
