neurological manifestations of scorpion sting
Transcript of neurological manifestations of scorpion sting
NEUROLOGICAL MANIFESTATIONS OF SCORPION STING
Scorpion sting is an acute life threatening , time limiting medical emergency
CASE
A 36 years old male patient non hypertensive, non diabetic was admitted to our hospital with h/o scorpion sting 3 days ago on the right little toe on 1/7/2011.
He developed excruciating pain locally followed by profuse sweating, vomiting, headache, within one hour of sting
After 2 hours patient became unconscious for 1 hour. On regaining consciousness patient was irritable and was unable to move left upper limb and lower limb and with facial asymmetry.
He was referred to our hospital after 3 days. On examination patient was irritable with GCS of E3M5V3 -11/15, profuse sweating, peripheries were cold, pulse rate of 100/minute and blood pressure of 100/70mm of Hg
Pupils 3mm, bilateral reacting normally with left hemiperesis (Power in left upper limb and lower limb 3/5). There were no local signs of sting.
During hospital stay patient had wide fluctuations of B.P ranging from 100/60mm of Hg to 160/90mm of Hg
Respiratory system, cardiovascular system examination was normal
INVESTIGATIONS
Hemoglobin – 13.8 gm%ESR: 20mm/1hrTLC: 15600/cummDifferential Leukocyte Count – N-89%, L-7%, M-4%Platelet Count: 2.82 lakhs/cumm BT-3 Min 30sec, CT: 7 MinsPT(T)- 13.6 Secs (Control 12.3)APTT - 32.9 Secs (Control-31.1)RBS – 130mg/dlECG: Normal sinus rhythm2D ECHO: No RWMA
Normal LV functionLVEF: 60%
He was treated conservatively (antioedema measures,adequate hydration, prazosin)
Patient improved sensorium wise after 3 days and became conscious, coherent and motor deficit improved after 1 week
CT SCAN BRAIN (PLAIN)
Hematoma in right frontal and left caudate with intraventricular extension
CT ANGIO
CT Angio is normal
SCORPION STING
INTRODUCTION
Out of 1500 scorpion species, 50 are dangerous to humans.
Scorpion stings cause a wide range of conditions, from severe local skin reactions to neurologic, respiratory, and cardiovascular collapse.
VARIOUS TYPES AROUND WORLD Buthus - Mediterranean area, from Spain to the Middle
East Parabuthus - Western and Southern Africa Mesobuthus – Throughout Asia Buthotus (ie, Hottentotta) - Across southern Africa to
southeast Asia Tityus - Central America, South America, and the
Caribbean Leiurus - Northern Africa and the Middle East Androctonus - Northern Africa to Southeast Asia Centruroides - Southern United States, Mexico
Among the 86 species of scorpions in India ,only 2 are of medical importance.
They are…Mesobuthus tamulus ( Indian red scorpion )Palamneus swammerdam (Black scorpion)
In general, scorpions are not aggressive. They do not hunt for prey; they wait for it.
Scorpions are nocturnal creatures They hunt during the night and hide in
crevices and burrows during the day to avoid the light.
Thus, accidental human stinging occurs when scorpions are touched while in their hiding places, with most of the stings occurring on the hands and feet.
Scorpions use their pincers to grasp their prey;
then, they arch their tail over their body to drive their stinger into the prey to inject their venom, sometimes more than once.
The scorpion can voluntarily regulate how much venom to inject with each sting.
The striated muscles in the stinger allow regulation of the amount of venom ejected, which is usually 0.1-0.6 mg
If the entire supply of venom is used, several days must elapse before the supply is replenished.
The potency of the venom varies with the species, with some producing only a mild flu and others producing death within an hour.
Generally, the venom is distributed rapidly into the tissue if it is deposited into a venous structure.
VENOM
Scorpion venom is a water-soluble, antigenic, heterogenous mixture, as demonstrated on electrophoresis studies.
This heterogeneity accounts for the variable patient reactions to the scorpion sting.
VENOM
Scorpion venom – toxins are polypeptides . Various enzymes are…..AcetylcholinesteraseAlkaline phosphataseAcid phosphatase5’nucleotidaseHyaluronidaseRibonuclease,deoxyribonuclease……
VENOM MECHANISM OF ACTION The primary targets of scorpion venom are
voltage-dependent ion channels, of which sodium channels are the best studied.
The long-chain polypeptide neurotoxin causes stabilization of voltage-dependent sodium channels in the open position, leading to continuous, prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic neurons.
This repetitive firing results in autonomic and neuromuscular overexcitation symptoms, and it prevents normal nerve impulse transmissions
Many end-organ effects are secondary to this excessive excitation.
VENOM MECHANISM OF ACTION Autonomic excitation leads to
cardiopulmonary effects. Somatic and cranial nerve hyperactivity
results from neuromuscular overstimulation. Additionally, serotonin may be found in
scorpion venom and is thought to contribute to the pain associated with scorpion envenomation.
VENOM MECHANISM OF ACTION
Furthermore, it results in release of excessive neurotransmitters such as epinephrine, norepinephrine, acetylcholine, glutamate, and aspartate.
Meanwhile, the short polypeptide neurotoxin blocks the potassium channels.
The binding of these neurotoxins to the host is reversible, but different neurotoxins have different affinities.
The stability of the neurotoxin is due to the 4 disulfide bridges that fold the neurotoxin into a very compact 3-dimensional structure, thus making it resistant to pH and temperature changes
PATHOPHYSIOLOGY
CLINICAL FEATURES
NEUROTOXIC LOCAL EFFECTS
Local evidence of a sting may be minimal or absent in as many as 50% of cases of neurotoxic scorpion stings.
A sharp burning pain sensation at the sting site, followed by pruritus, erythema, local tissue swelling, and ascending hyperesthesia, may be reported.
This paresthesia feels like an electric current, persists for several weeks, and is the last symptom to resolve before the victim recovers.
Hyperthermia Tachypnea Tachycardia Hypertension Arrhythmia Pulmonary edema Hyperglycemia Diaphoresis Piloerection Restlessness and
apprehension Hyperexcitability and
convulsions
Bronchoconstriction Bradycardia Hypotension Salivation, lacrimation,
urination, diarrhea, and gastric emesis (SLUDGE)
Rhinorrhea and bronchorrhea
Goose pimple skin Loss of bowel and bladder
control Priapism Dysphagia Miosis Generalized weakness
SYMPATHETIC PARASYMPATHETIC
AUTONOMIC EFFECTS
CRANIAL NERVE EFFECTS
Classic roving or rotary eye movements Blurred vision Tongue fasciculations Loss of pharyngeal muscle control Difficulty swallowing Excessive salivary secretions Respiratory difficulty.
CENTRAL NERVOUS SYSTEM
Infrequently encountered but invariably fatal. Encephalopathy, Convulsions within 1-2 hours of sting Stroke -both cerebral hemorrhage and thrombosis Central respiratory failure
These manifestations are similar to strychnine like effect and spurt of BP secondary to catecholomine release occasionally leads to rupture of intracerebral artery resulting in intracerebral bleed and also cerebral infarcts due to thrombosis due to coagulant nature of venom and autonomic storm induced vasospasm
SOMATIC EFFECTS
Rigidity and spasticity in muscles of the
limbs Involuntary muscle spasms Twitching Clonus and contractures Alternating opisthotonous from inactivation
of sodium channels, leading to increased sodium and calcium uptake
Increased tendon reflexes, especially prolongation of the relaxation phase
Piloerection accompanied by goose pimples
The signs of the envenomation are determined by the scorpion species, venom composition, and the victim's physiological reaction to the venom.
The signs occur within a few minutes after the sting and usually progress to a maximum severity within 5 hours.
The signs last for 24-72 hours and do not have an apparent sequence.
Thus, predicting the evolution of signs over time is difficult.
Furthermore, a false recovery followed by a total relapse is common.
CARDIOVASCULAR Myocarditis Gallop rhythm Hypertension or hypotension Arrythmias Conduction blocks Myocardial infarction Congestive heart failure Shock Pulmonary edema
Develop within 30 min to 3 hours after a sting due to myocardial dysfunction
RESPIRATORY
Dyspnea Cyanosis Hemoptysis ARDS
GASTRO INTESTINAL
Acute pancreatitis - intra-pancreatic conversion of trypsinogen to trypsin
Pseudo pancreatic cyst Rise in liver enzymes Necrosis of liver
RENAL
Hematuria Oliguria Acute renal failure
METABOLIC
Acidosis Hyperglycemia Hyperkalemia Raised free fatty acids Raised cholesterol & triglycerides
SYSTEMIC INFLAMMATORY RESPONSE
SIRS is triggered due to increased levels of Interleukin -6 IL-1a IL-1beta IFN-gamma Alpha 1-antitrypsin
GRADING OF SEVERITY
Santhana krishnan grading GRADE 1 –peripheral circulatory failure good GRADE 2 – GRADE 1 + myocarditis prognosis GRADE 3 – GRADE 2 + CNS failures
MANAGENENT
SUPPORTIVE
ABC O2 inhalations Inj TT Benzodiazepines NSAIDS Local ice packs Xylocaine infiltration IV fluids
MANAGEMENT
Prazosin–A competitive post-synaptic alpha1,
adreno-receptor antagonist–should be the first line of management
Suppresses sympathetic outflow Activates venom-inhibited potassium
channels. Decreases the preload, afterload and blood
pressure without increasing the heart rate. Reverses the metabolic and hormonal effects
of alpha receptors stimulation
By accumulating c GMP counters vasoconstriction induced by
endothelins prevents further myocardial injury
Peak concentration is reached in 1-3hours and plasma half life is about 2-3hours. Clinically, it starts acting in 1 hour and maximum action occurs at the end of three hours.
Prazosin is a cellular and pharmacologic antidote to the actions of scorpion venom and it is also cardioprotective.
DOSAGE
Available as 1 mg/2.5mg/5mg tablets. The dose recommended is 30
microgram/kg/dose Sustained release tablets are not
recommended in this condition. Prazosin repeated in the same dose at the
end of 3 hours according to clinical response And later every 6 hours till extremities are
warm, dry and peripheral veins are visible easily
SVIMS Experience: Oral L-carnitine is useful to treat patients with scorpion ting envenomation, myocarditis and shock (Rajasekhar D, Mohan A. Natl Med J India 2007)
It should not be given as prophylaxis in children when pain is the only symptom. First dose phenomenon
Can be given irrespective of blood pressure
provided there is no hypovolemia The time lapse between the sting and
administration of prazosin for symptoms of autonomic storm determines the outcome
L-CARNITINE
SVIMS Experience: Oral L-carnitine is useful to treat patients with scorpion ting envenomation, myocarditis and shock
(Rajasekhar D, Mohan A. Natl Med J India 2006)
SCORPION ANTIVENOM
Scorpion venoms reach their target too rapidly to be neutralized and anti-venom within 30 minutes of sting may reverse their effect
Antivenom against the toxins of Indian scorpions is not available for clinical use
UNHELPFUL RX
Lytic Cocktail (Pethidine + Promethazine + Chlorpromazine )
Morphine Steroids Atropine Nifidepine Ace Inhibitors (Captopril)
COMPLICATIONS
Dilated cardiomyopathy Ankylosis of small joints if the sting occurs at a
joint Rhabdomyolysis Persistent paresthesias Antivenin anaphylaxis and serum sickness Respiratory arrest Cardiac arrest Shock Seizures Death
PROGNOSIS
In the pre-prazosin era (1961-1983), 25-30% fatality due to pulmonary edema was reported in scorpion victims
Since the use of prazosin (1984 onwards) the mortality in these victims is reduced to less than 1%
KEY MESSAGES
Scorpion venom is a potent sympathetic stimulator Cardiac manifestations are common in Indian red
scorpion envenomation Both hemorrhagic and ischemic strokes are known to
occur CNS involvement indicates poor prognosis Alpha receptors stimulation plays a major role in
evolution of myocardial dysfunction and acute pulmonary edema in victims of scorpion sting
Prazosin–an alpha adrenoreceptor antagonist–is antidote to venom action
Time lapse between the sting and administration of Prazosin for autonomic storm determines the outcome
REFERENCES1) Rai M. Intracerebral hemorrhage following scorpion bite.:Neurology. 1990;40:1801
2) Udayakumar, N, Rajendiran, C, Srinivasan, AV. Cerebrovascular manifestations in scorpion sting: a case series. Indian J Med Sci 2006; 60: 241–244.
3) Raichur, DV, Magar, VS, Wari, PK, Chandragouda, DK. Hemiplegia and motor aphasia following scorpion sting. Indian J Med Sci 2001; 68: 669–670
4) Bonilha, L, et al. Epilepsy due to a destructive brain lesion caused by a scorpion sting. Arch Neurol 2004; 61: 1294–129
5) Bawaskar HS, Bawaskar PH. Scorpion sting. J Assoc Physicians India. 1998; 46: 388 – 392
6) Kavathale, Khan A et al. Scorpion – Stings the limb and stuns the heart? J Assoc Physicians India 1999; 47: 1045 – 1046
7) Sundararaman T, Olithselvann M et al. Scorpion envenomation as a risk factor for development of dilated cardiomyopathy. J Assoc Physicians India 1999; 47: 1047 – 1050
8) Elatrous S et al. Dobutamine in severe scorpion envenomation. Effects on standard haemodynamics, right ventricular performance and tissue oxygenation. Chest 1999; 116: 748 – 753
9) Bawaskar HS, Bawaskar PH. Prazosin therapy and Scorpion envenomation. J Assoc Physicians India. 2000; 48: 1175 – 1180
10) Natu VS et al. Efficacy of Species Specific Anti-scorpion Venom Serum (AScVS) against severe serious scorpion stings ( Mesobuthus tamulus concanesis Pocock) – an experience from Rural Hospital in Western Maharashtra. J Assoc. Phys of India 2006; 54: 283 - 287