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Creutzfeldt-Jakob Disease (CJD) is a relatively rare cerebral disorder involving rapid decrease of mental function and movement known to be caused by abnormal brain proteins called “prions”. It is the most frequent human variety of prion diseases and similar to the various transmissible spongiform encephalopathies that afflict animals including the new variant “Mad Cow Disease” (nv CJD). Prions cause devastating changes in the CNS particularly the grey matter causing neuronal loss, gliosis and diffuse fine-meshed vacuolation of the neuron containing structures.

The yearly incidence is about 1 in a million. Creutzfeldt & Jakob in the early 1920’s described six cases of human progressive dementing illness with spasticity, ataxia and involuntary movements. Bjorn Sigurdsson termed slow infection in 1954 with reference to a chronic degenerative disease of brain in sheep known as scrapie. In 1957 Gajdusek and Zigas described the illness among the fore people of Eastern New Guinea practicing ritual cannibalism. In 1982 Prusiner coined the term “prion” to describe the unconventional pathogen.7 All prion disorders are associated with aberrant metabolism of PrP, the prion protein. However, in India the first case of CJD was reported in 1965 and since then sporadic cases have been reported very often.8

We report such a relatively rare case from western Orissa with great deal of diagnostic difficulties at the out set.

S.B., a 68 year old female was admitted to a local hospital for failing memory and behavioral changes followed by lack of co-ordination and visual disturbances. She was provisionally diagnosed to be a case of Alzheimer’s Disease in early 2002. Gradually she noticed pronounced mental deterioration and involuntary movements and weakness of extremities with altered sensorium for which she was admitted to a central hospital and was treated on the line of cerebrovascular accident. On 12th February 2003 she was referred to V.S.S. Medical College, Burla for further treatment.
There was no past history of similar illness / phychiatric or neurological disorder. There was history of cataract operation with intraocular lens (IOL) implantation in August 2002. But there was no history of vaccination in the recent past. She was a newly detected diabetic and hypertensive but under control. She was married and blessed with two children, non-vegetarian by diet (no history of beef or pork intake) and no history of addiction of any kind. Family history was not suggestive.
The patient was stuporus, non-communicative, feebly responsive to painful stimuli, pulse rate 86/pm, regular, BP 130/80mmHg, afebrile, per abdomen, CVS and respiratory system revealed no abnormality.
CNS examination revealed stiffness in all the limbs, deep tendon reflex increase, myoclonus present with flexor plantar response.
Routine investigations showed Hb-11.5gm%, MP (QBC)-negative, TLC-10000/mm3, ESR-15mm, FBS-86 mg%, Serum Na + 138, Serum K + 4.3, Blood urea – 67 mg%, Serum creatinine – 1.05 mg%. CSF, urine examination and ECG were within normal limit.

CT Scan (Fig.1) was normal. The EEG (Fig.2) revealed presence of periodic complexes at an interval of less than one/second arising from both sides, which was characteristic of C.J. disease.
She was initially treated on the line of metabolic encephalopathy. During follow up the patient developed generalized tonic clonic seizures next day of admission but was controlled with anti-epileptic medication. However, there was gradual deterioration of neurological status and she died on 22-02-03 after about 10 days of hospital stay.
Sporadic form of CJD is the most frequent variety presenting spontaneously, not transmitted from person to person.6 Familial form is transmitted as autosomal dominant inheritance in 15% cases due to a point mutation in the gene encoding PrP at codon 178 producing asparagine.3 Iatrogenic form results with corneal transplants, dural grafts, intracerebral EEG recordings and recipients of human growth hormone in growth failure cases, although the incidence after cataract operation and IOL implantation have not been reported.
The clinical tetrad of CJD is subacute progressive dementia, myoclonus, typical periodic complexes on the EEG and a normal CSF.7 The cognitive impairment may be quite global in nature as evidenced by neuropsychological testing. Prodromal symptom experienced in approximately 1/4th of patients may occur weeks to months preceding onset of progressive dementia, which is the hallmark of the illness.4 Ataxia seen in 1/3rd of patients initially but ultimately occur in as many as 70% cases. In about 10% of patients the illness begins with almost stroke – like suddenness and runs its course rapidly in a matter of few weeks or months.
Heidenhain’s variant of CJD includes cortical blindness and visual agnosia where as in Brownell and Oppenheimer variant cerebellar ataxia with a relative paucity of cognitive impairment (17%) dominates, Dyskinesias, prominent extrapyramidal features, seizure, LMN features, autonomic dysfunction, stroke-like presentations and supranuclear gaze palsies are some of the exceptional presentations.7 Jakob type of CJD is the cortio-striato-spinal variant where as the lesion in the diffuse variety (Stern and Garcin) lies in the basal ganglia and thalamus. Besides in the panencephalitic form there is involvement of white matter out of proportion to the degeneration of grey matter.4
Only the electro-encephalogram is of diagnostic significance amongst all routinely available laboratory studies. In well advanced disease 1-2 cycles per second triphasic sharp waves superimposed on a depressed background are characteristic. These periodic sharp waves are asymmetrical tend to become slower with progressive course of the disease. This is evident within 3 months of onset in approximately 80% cases. A non-specific abnormality in the form of symmetrical theta and delta waves on an irregularly depressed background may be seen before the occurrence of periodic sharp waves in about 50% cases. Often episodic burst suppression high voltage activity is seen which is less specific and rare during the early course.5
CFS parameters are usually normal and imaging studies of brain remain normal in majority of patients. Cerebral atrophy may be noted occasionally on MRI.1 Positron emission tomography (PET) in few cases shows regional hypometabolism of glucose reflecting loss of neuronal function. Brain biopsy specimen for neuropathologic study is the definitive diagnosis revealing a fine-meshed spongy vacuolation and should be carried out if thought by the physician with due consent by family members as the disease is invariably fatal. However, a finding of normal tissue morphology does not exclude the disease and in such situation typical EEG abnormality can lead to a correct diagnosis.2
As such caution should be maintained while operating for cataract and if any IOL is planned for the patient, the transmission of CJD should be kept in mind.
1. Esmonde TFG : Will RG MRI in CJD : Ann. of Neurology, 1992; 31:230-1.
2. Gertz HJ; Henker H : Cervos Navarro J : CJD disease : correlation of MRI and Neuropathological findings : Neurology : 1988; 38 : 1481-2.
3. Goldfarb LG, Petersen RB, Tabaton et al, Fatal familial insomnia and familial creutz feldt Jakob disease : Disease phenotype determined by DNA polymorphism. Science : 1992:258:806-8.
4. Kretzschmar HA : Human prion Diseases (Spongiform encephalopathies) Arch Virol supplementum : 1993; 7:261-293.
5. Levy SR, Chiappa KH, Burke CJ, Young RR. Early evolution and incidence of EEG abnormalities in CJD. J. Clinic. Neurophysiol. 1986; 3 : 1 – 21.
6. Masters CL, Gajdusek DC : The spectrum of CJD and the virus inducd subacute spongiform encephalopathies. In Smith WT, Cavanagh JB (Eds) Recent Advances in Neuropathology, Churchill Livingston, Edinburgh 1982: p-139.
7. Prusiner SB, Human Prion Diseases : Ann. Neurology, 1994a; 35:385-95.
8. Shankar SK; Satish Chandra P : Creutz feldt Jakob disease in India – A report Neurology India : 1988; 36, 279-283.

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Symmetric peripheral gangrene (SPG) is a rare clinical presentation in case of falciparum malaria. Few cases have been so far reported from India and abroad. Here we report such a case from this hospital and discuss the pathophysiology and management.


Symmetric peripheral gangrene (SPG)
Falciparum malaria
Disseminated intravascular coagulation (DIC)


SPG is an uncommon clinical condition characterized by sudden onset of symmetric dry gangrene of acral distribution without any evidence of vasculitis or arterial obstruction. This has been described in conditions like infections most commonly bacterial (meningococcal, streptococcal, Pneumococcal, E.coli septicaemia) and viral (varicella and viral gastroenteritis), low output states like myocardial infarction, shock, CCF or use of drugs like vasopressin and ergot and other conditions like polymyalgia rheumatica,cryoglobinaemia. In all these conditions DIC has been the basic pathogenesis (90%)9.

The incidence of DIC and SPG in cases of falciparum malaria has rarely been reported as one of its multiple complication1.

A 15 years boy from Raigarh (C.G.) admitted to this hospital in last week of December 2005 with history of fever associated with chill and rigor (20 days), sudden blackening of distal parts of fingers, toes of all limbs , tip of nose and lateral part of pinna of both ears (15 days) and altered sensorium for 3 days. He was treated at the local hospital with I/V fluid, antibiotic and decadron , without any improvement.

There was no history of joint pain, trauma, sore throat, spontaneous bleeding, thromboembolic episode or any relevant disease like SCD, HTN, DM. He was a student in a residential school without habit of smoking or alcohol. There was no relevant family history.

On examination the patient was stuporous with Temperature 1000F , pulse – 100/min , regular low volume and all the peripheral pulsations well felt without brachiofemoral delay. BP was 110/70 mm of Hg (both U/L), with moderate pallor and features of dehydration. There was no icterus , clubbing, lymphadenopathy or thyromegaly. Cardiovascular and Respiratory system revealed no abnormality. There was no hepatosplenomegaly. Neurological examination revealed mild neck rigidity with diminished DTJ and plantar was flexor. Examination of skin and digits showed blackening of tip of nose (Fig.1), both ear pinna on lateral aspects (Fig 2) and distal parts of toes and fingers of all limbs (dry gangrene) (Fig 3 & 4). There was clear line of demarcation between the healthy and affected parts.

Investigation on the day of admission showed
Hb: 6.2 gm%
DC : N - 48, E-2, L-48, M-2, B-0
TLC: 9800/mm3
TPC: 60,000/mm3
RBS : 116mg%
B. Urea : 96mg%
Serum Creatinine : 1.5mg%
Blood smear : Showed P.falciparum rings and gametocytes
Serum Bilirubin : Total 0.78mg%
Direct 0.26mg%
SGPT : 36U/L
Alkaline phosphatase: 50U/L
Electrolytes: Serum Na+ - 138meq/L
Serum K+ - 3.6meq/L
Serum Ca++ - 8.5 mg/dl
Prothrombin time (PT) – 16 second (control 12.5)
Activated partial thromboplastin time (aPTT) 29.5 seconds (control – 28)
Fibrinogen : 187mg/dl (N : 250-450mg/dl)

The patient was treated with injection Artesunate, injection Ceftriaxone 2gm I/V BID,injection Omnacortil, Injection Ranitidin 8 hourly, I/V fluid and tablet Zilast (Cilostazol 100mg BID) with care of the skin , bladder, bowel and maintaining nutrition. He was stabilised on 2nd day and gained consciousness and there was clinical improvement. Two units of whole blood transfusion given.

On further investigation urine analysis was normal and haemoglobin electrophoresis was AA (to exclude SCD – common in this belt). USG of abdomen and pelvis was normal. Test for antinuclear factor, LE cell, Rheumatoid factor, VDRL were negative, Test for cryoglobulin was normal. Coagulation profile (Antineutrophil cytoplasminc antibodies, Antinuclear antibodies, anti double standard DNA, complement –3 , complement – 4) was normal. Serum uric acid was 3.9 mg/dl.

Echocardiography did not reveal any thrombi or vegetation. The Doppler study of the vessels demonstrated normal flow pattern upto digital arteries in all four limbs.

Biopsy of an affected area of the skin showed thrombi in dermal capillaries without any evidence of vasculitis.

Blood could not be tested for fibrin degradation products (FDPs). However evidence of DIC was seen in skin biopsy.

Gradually the patient improved. Full anti-malarial course was given and antibiotic was given for 7 days. Zilast was continued and omnacortil was gradually tapered. Slowly the gangrenous parts improved and patient was discharged on 12th day. No surgical intervention was required.

SPG has been reported in various medical conditions including falciparum malaria1, 7, 4, 2, 6,12. Our patient had no clinical or laboratory evidence of other causes like sepsis, vasospastic condition, ergot or other drugs. There was no evidence of vasculitis, cryoglobulinaemia, polycythemia or thrombocythaemia. The common pathogenic mechanisms of SPG is DIC9. All the cases reported had evidence of DIC.

Reduced fibrinogen level, thrombocytopenia, prolonged PT, prolonged aPTT and histopathological evidence of microvascular thrombi indicate the presence of DIC in this patient1.

Alteration of coagulation and fibrinolytic system in falciparum malaria is well recognized5. A functionally active but controlled coagulatory state exists in falciparum malaria even in uncomplicated cases5. Elevation of FDPs reflecting the ongoing fibrinolysis have been documented11. Heavy parasitaemia triggering the coagulation pathway10, alteration in the lipid distribution across the surface membrane of the parasitized erythrocytes activating the intrinsic coagulation cascade8 and activation of complement system5 have been postulated as possible mechanism for DIC in falciparum malaria. Sequestration of the parasitised erythrocytes in the microcirculation by molecular interactions with endothelial receptors, mainly intracellular adhesion molecule10 – 1(ICAM – 1) may occur. Rosetting of the healthy erythrocytes around parasitised red cells may occur and these multicellular aggregates further exacerbate the vascular obstruction caused by sequestration3.

DIC is encountered in less than 10% of patients with cerebral malaria3 and manifest as spontaneous bleeding from gum and GIT. But in a review of 71 cases of SPG and DIC significant bleeding complications were not recorded9.

Our patient who had no other cause of peripheral gangrene made satisfactory recovery on specific antimalarial therapy supporting the observation that falciparum malaria was the triggering mechanism for the DIC and subsequent SPG.


In conclusion we report that falciparum malaria may present as peripheral dry gangrene and this possibility though uncommon must be taken into consideration while encountering patients in endemic areas.

1. Anuradha S, Prabhash K,Shome DK et al . Symmetrical peripheral gangrene and falciparum malaria an interesting association. JAPI 1999; 47(7): 733-5.
2. Arya TVS, Singh SP, Singh DK. Bilateral foot gangrene occurring in falciparum malaria. JAPI 1990; 38: 30 (Abstract).
3. Bradley D, Newbold CI, Warell DA. Malaria in Oxford Test Book of Medicine. Weatherall DJ Ledinqham JGG and Warrell Da (eds) Oxford University Press Inc. New York 1996; 1 : 835-63.
4. Chittichai P, Chiekrul N, Davis TM. Peripheral gangrene in nofatal paediatric cerebral malaria: a report of two cases. Southeast Asian Trop Med Public Health 1991; 22: 190 – 4.
5. Clemens R, Pramoolsinsap C, Lorenz R et al . Activation of coagulation cascade in severe falciparum malaria through the intrinsic pathway.Br. J. Haemat. 1984; 87,100-05.
6. Jain D, Srivastava S, Singhal SS. A rare presentation of falciparum malaria . JAPI 1995; 43: 582.
7. Kochar DK, Shubhakaran , Kumawat B et al. A patient with falciparum malaria and bilateral gangrene of the feet who developed arrhythmia/ventricular fibrillation after quinine therapy. Quart J Med 1998 (Corrosp)246.
8. Mohanty D, Marwah N, Gosh K et al. Vascular occlusion and disseminated intravascualr coagulation in falciparum malaria. Br. Med J 1985; 290: 15-6.
9. Molos MA, Hall JC. Symmetrical peripheral gangrene and disseminated intravascualr coagulation. Arch Dermatol 1985; 121: 1059-61.
10. Philips RE, Looareesuwan S, Warrell DA Et al . The importance of anemia in cerebral and uncomplicated falciparum malaria: role of complications dyserythripoiesis and iron sequestration. Quart J Med 1986; 58: 305 – 23.
11. Rojanasthein S, Surakamolleart V, Boonpucknavig S et al . Hematological and coagulation studies in malaria. J. Med Assoc. Thai 1992; 75 (supplele-1):190-4.
12. Sharma BD, Gupta B. Safdarjung Hospital, JIACM 2002, 3(3): 297 – 9.

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Fish is a very common and tasty food and at the same time very nutritious too. There have been many cases of food poisoning after intake of poisonous fishes. Here we report one such case where 8 people got admitted to V.S.S. Medical College Hospital, Burla after consuming some kind of fish developed signs and symptoms of tetrodotoxin food poisoning. Among those 8 patients 2 of them expired.

Food poisoning, Ich thyotoxicosis, Tetrodotoxin, Puffer fish

Fish is a very delicious food throughout the world, which is widely consumed. There are two categories of fishes-marine and fresh water. Few people know about the toxins present in the fish of both categories. The poisonous fishes are morphologically different from other edible fishes. The study of toxin of fish is known as Ichthyotoxicosis which is an important part of food poisoning. It is very important to know the toxins present in the fish so that fish can be taken as healthy food.

Here is an important case of food poisoning consumed by local tribals and admitted to V.S.S. Medical College Hospital and the end result is described below.

On 18/10/2007 total eight people came to casualty around 8.30PM with history of taking one kind of fish in a social function. Locally known as “Fukka” and their signs and symptoms which developed within half an hour of intake such as paresthesia, vomiting, abdominal pain, breathlessness, dysphagia and extreme weakness of 4 limbs. In past history there was no history suggestive of diabetes mellitus, hypertension, sickle cell disease, bronchial asthma. In personal history there was no history of any addiction and they were from poor socioeconomic status.

The common clinical signs presented in such patient are respiratory rate: 25-30/min, BP - 100/70 to 110/80 mm of Hg , Pulse rate- 96- 104 /min regular and low volume. Per abdominal examination no abnormality detected. Chest examination bilateral vesicular breath sound and no added sound. Cardiovascular examination revealed first and second heart sounds normal and no murmur heard. The central nervous system examination revealed patients irritable and anxious with ptosis (B/L), pupils (B/L) normal in size and normally reacting to light, tone of the muscles of limb decreased and power of muscles of limbs Grade 2, plantar no response (B/L) and no meningeal signs.

On investigation of the patients Hb – 10-12gm%, ESR - 6 -10 mm (1st hour) DC, TLC within normal limit. Serum creatinine 0.8 – 1.0 mg/dl, blood urea 26-34 mg/dl, serum Na+ 136-140 meq/L, Serum K+ 4.0 – 4.6meq/L, urine routine and microscopic examination within normal limit. Random blood glucose 140mg/dl and ECG within normal limit.

The following treatment was given like stomach wash with KMno4, Oxygen inhalation, injection atropine and injection neostigmine alternately every 15 minute, injection ceftriaxone and injection hydrocortisone (100mg) IV 8 hourly, injection deriphylline 1 ampoule IM 8 hourly, injection ranitidine 1 ampoule IV 8 hourly, IV fluids, cathetrization of bladder and ryles tube were administered under sterile technique.

Course of treatment:
Out of 8 patients 2 became very serious like respiratory distress with laboured and hurried respiration along with frothing from mouth and coarse crepitations heard bilateral in lung fields. The 2 patients became stuporous leading to coma and death at 8 AM next day in spite of cardiopulmonary resuscitation. The signs and symptoms of other 6 improved gradually and they had an uneventful recovery and were discharged after 4 days.

Postmortem findings:
The two cases were subjected to medicolegal autopsy and the autopsy findings were:

External features: Face livid, frothy, blood tinged discharges from nostrils, eye closed, pupil dilated and fixed, nail bed cyanosed, rigor mortis all through the limbs.

Internal features: In both case stomach contained 100ml of brownish liquid, the mucus membrane were congested without excoriation. Liver, spleen, kidney were intensely congested. Right chamber of heart contained clotted blood and left chamber empty, great vessels were empty. The cause of death was established as asphyxia as a result of respiratory failure.

The final cause of death was pending chemical examination of visceras. For that stomach with its content, 500 gm of liver, intestine 30 cm and half of each kidney were preserved in saturated solution of common salt and handed over the police to further transmission to chemical examination.

The relative were advised to bring the particular fish which they have consumed and the fish was identified as puffer fish (Photo 1, 2).

The fish consumed by eight people were identified to be Puffer fish after morphological examinations of the fish they have brought. Its local name is “Fukka”. In Japan a local variety of Puffer fish called “Fugu” is considered a delicacy but it requires special training and licensing of preparation as they are poisonous1. These fishes contain a toxin known as tetrodotoxin which is a heat stable, non protein neurotoxic predominantly concentrated in ovaries, kidneys , fish skin, muscles and intestine of Puffer fish2. Describing in detail tetrodotoxin is water soluble and its chemical nature is aminoperhydroquanizole1.

The ovary’s high concentration of the toxin renders female more poisonous during spawning season7. The toxin can be detected by mouse bioassays and fluroscent spectrometry1. The tetrodotoxin resembles another toxin called saxitoxin, from which it is distinguished by heat stability up to 1000C in acidic medium5.

The action of tetrodotoxin is more prolonged but saxitoxin is more neurotoxic5. Neurotoxicity of tetrodotoxin is due to inhibition of sodium potassium pump activity and blockade of neuromuscular inhibition1. The blockade at motor end plate is competitive and reversible2.

The clinical features of tetrodotoxin fish poisoning begins shortly after ingestion (10-45min) such as paresthesia of the lips, face , toes and fingers, vomiting, light headedness, feeling of doom, diaphoresis, dysphagia and dysarthria2. Buccal bullae, salivation, cranial nerve palsies and even convulsion have been reported1. An ascending paralysis develops with respiratory paralysis as a preterminal event (6-24 hours) of post ingestion2. In serious poisoning hypotension, cardiac dysarythmias like bradycardia were also observed1.

Diagnosis is mostly done from history and clinical presentation and treatment is mostly symptomatic and supportive7. Removal of toxin by stomach wash, IV edrophonxium or IM neostigmine restores muscle strength2. Airway intubation and ventilators are necessary if patients develops respiratory paralysis6. Studies have shown that mortality has approached 60%2.

Burla is situated on the bank of river Mahanadi. In past 2 years zoologist have found out that in river Mahanadi and its tributaries there is increase in tetrodotoxin containing fishes which were not seen 10 years ago. This is because of favourable temperature and pH of water of Mahanadi and its tributaries that caused an explosion of population of puffer fishes. This is because of construction of various factories in nearby areas for which the flora and fauna of Mahanadi river is getting rapidly destroyed and along with there is decreased species of fresh water fishes in resorvior (Dainik Samaj 01/11/2007).

In spite of fish being a very much proteinous food it can kill human beings with its toxins as described above. It is a staple food in costal districts of Orissa, which cannot be replaced with any other food because it contains excellent and excessive protein. So we have to take some prevention for abetting the toxin found in the fish.

Tips to prevent fish poisoning:
1. Avoid eating large tropical fish like shark, barracueda, red snapper, dear bass etc5.
2. Do not consume fish that are likely to have decomposed i.e. fish that have not been stored or preserved properly5.
3. Do not eat the viscera of fish (particularly liver and gonads). See that the fish is properly cleaned and cooked5.
4. It has been suggested that suspect fish be first fed to a cat. If the cat dies within 8 hours, it is an explicit indication that fish is toxic5.
5. Do not eat unidentified fishes.
1. Gold Frank’s Toxicologic Emergencies, 6th Edition, P 1169-1170 by Lewis R Goldfrank, Neal E Flomenbaum, Richard S Weisman, Mary Ann Howland, Rober S Hoffmann, Neal A Lewin.
2. Medical Toxicology Diagnosis and Treatment of human poisoning Pg 1197-1198 by Mathew J Ellenhorn , Donald G Barcelous.
3. Modi’s Medical Jurisprudence and Toxicology, 23rd Edition by K Mathiharan & Amrit K Pattnaik.
4. Modern Medical Toxicology by V.V. Pilli.
5. Mosher HS, Fuhrman FA, Buchwald HD et al; Tarichatoxin – tetrodotoxin , A potent neurotoxin science 1964; 44; 100-1110.
6. Sims JK, Ostman DC, Puffer Fish poisoning : Emergency diagnosis and management of mild human tetrodotoxication: Ann Emerg Med 1986; 15:1094-1098.
7. Torda TA, Sinclair E, Ulyatt DB, Puffer fish (Tetrodotoxin)poisoning clinical records and suggested management. Med J Aug 1973; 1: 599-602.

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Hydatid cysts are due to parasitic infection caused by the cestode tapeworm Echinoccocus. In humans the hydatid disease commonly involves the liver (75%) & the lungs (15%). The remaining (10-15%) cases involve the other organs of the body-kidney, spleen, heart, brain, bones, pancreas, breast, ovaries, scrotum, thyroid gland, inguinal canal & soft tissues.The disseminated intra-peritoneal hydatid disease is a very rare finding1. We report such a case wherein the abdominal cavity is seen to contain multiple hydatid cysts .Hydatid cysts were also found in the left scrotum, lungs, liver & spleen.

Hydatid cyst, Echinococcus, Peritoneal hydatidoses, Scrotum

A 42 years Hindu male presented with complaints of left scrotal swelling for 6 months, progressive distention of abdomen for 1 year & generalized weakness for 1 ½ years. He had past history of hydatid disease 13 years back, for which cystectomy was done in 1994. He was not taking any drugs. There is no history suggestive of diabetes mellitus, hypertension, tuberculosis, coronary artery disease or history of Filariasis.

On examination, patient was of thin built with blood pressure 110/70 mmHg (both upper limb), pulse rate 84/min (Regular), Respiratory rate of 24/min and temperature of 37oC. He had diminished vesicular breath sounds in both lower lung fields. His abdomen was distended. On inspection, dilated veins were present over the abdomen with flow below upwards. There was a mid line supraumblical scar mark. Flanks were full and contour was irregular. Umblicus was central and everted (Figure 4). On palpation, there was no local rise of temperature, no tenderness, no fluid thrill and shifting dullness. There were multiple ill defined cystic masses all over the abdomen of varying size. There was bilateral scrotal mass which was soft and non-tender with increased scrotal volume. The liver was not enlarged and spleen was not palpable. On auscultation, bowel sound was normal, no bruit heard. Cardiovascular system and central nervous system examinations were within normal limit.

Hb%-10.4gm%, TLC-12,000/mm3, N50E28L22, ESR-48mm(1st hours), FBS-74mg/dl, Blood urea-31mg/dl, Sr creatinine-1.58mg/dl, Sr Na+-143meq/lt, Sr K+-4.9meq/lt, Urine analysis-normal study,ECG-normal.

Sr Billirubin (total)-0.89mg/dl, Direct-0.22mg/dl, Indirect-0.67mg/dl, SGOT-26.39IU/lt, SGPT-18.40IU/lt, Sr Alkaline phosphatase-149.38IU/lt, HBsAg-negative, Anti HCV Ab-negative.

Multiple hydatid cysts of liver, spleen, left scrotum & through out abdomen, varing from size 1 mm to 6 mm, B/L moderate Hydrocele (Figure 3).

Circular opacity of size 8x2cm in right basal zone (? hydatid cyst).

Multiple hydatid cyst of liver, spleen, B/L lower lobes of lungs, involving mesentery & retoperitoneal region. Nonvisualization of RT kidney
(? replaced by hydatid cysts) (Figure 1, 2).


Echinococcus antibody titer - 1:64 (Normal 1:32)

Surgical resection of the cysts was not possible. Albendazole-400 mg PO BD for life long (with monthly monitoring of Liver function Tests) given. On first two follow ups there was decrease in the abdominal distension & the liver function test was normal.

Hydatid disease is a parasitic infection caused by the Echinococcus granulosus. The dogs are the definite host and the adult worms are found in their small intestine. Human get infected either by contact with the definitive host or by consuming vegetables and water, contaminated with the hydatid ova2. Hydatid disease is endemic in the cattle grazing areas like India, Pakistan, Middle-East, Africa, South America, and New-zealand1. The close association of people with sheep and dogs and the unavailability of clean potable water supplies in India make it a region endemic to disease. Majority of the cases of Hydatid disease seen come from rural areas or people who have settled in urban centers after spending life in villages. Most of the people acquire the disease during their childhood, but do not present with the clinical signs and symptoms until late adult hood. The natural progression of an untreated cyst may include calcification and death of the cyst; however, more frequently the cyst gradually enlarges3.

The liver (75%) and the Lungs (15%) is the commonest site of involvement, although no site in the body may be completely immune from it4. This atypical and rare presentation of the disease may be seen in kidneys (3%), usually the upper and the lower pole of the kidney may be involved. The spleen may be involved in about 4% of the cases and is associated with splenomegaly, fever and abdominal pain4. Cerebral Hydatid cysts occur in only 2% of all the cases reported. The region of the middle cerebral artery distribution specially the parietal lobe is most frequently involved. Cardiac Hydatid cyst is very rare (0.02-2%) and most commonly affects the left ventricular chamber specially the left ventricle in 50%-60% of cases4. The other sites that have been reported to be involved are bones, pancreas, breast, ovaries, scrotum, thyroid glands, inguinal canal and soft tissues.

Hydatid cysts can also be found rarely in the peritoneum1. Most of these cases are the result of traumatic or surgical rupture of a hepatic, splenic or mesenteric cyst. The prevalence of peritoneal hydatid cysts in cases of abdominal Hydatid disease is approximately 13%. In our case the patient had already undergone cystectomy and it is likely that these findings may be associated to previous surgical rupture, although spontaneous rupture of micro cysts into the peritoneum may also occur in about 12% of the cases1. The hydatid cysts may resemble a multiloculated mass filling the entire peritoneal cavity. Such a condition is referred to as peritoneal hydatidoses .

Hydatid cyst may be solitary or multiple. The type of the imaging modality used depends on the site and the size of the hydatid cyst. Ultrasonogarphy (USG) is the first line of screening for abdominal hydatidosis and it is especially useful for detection of cystic membrane, septa, and hydatid sand. CT scan best demonstrates cyst wall calcification and cyst infection. CT scan imaging is also the modality of choice in peritoneal seedling1. The CT scan shows well defined solitary or multiple cysts that may be thin walled or thick walled. A hydatid cyst typically demonstrates a high attenuation value at unenhanced CT even without calcification. Multivesicular cysts can depict a typical honeycomb pattern. The septa represent the walls of the daughter cysts housed within the mother cyst. A “wheel spoke” pattern can be observed when the daughter cysts are separated by hydatid matrix1.

There are different types of serological tests which can be carried out for the diagnosis, screening and follow up of patients with hydatid disease. These include the immunoelectrophoresis, enzyme-linked immunosorbent assay (ELISA), latex agglutination and indirect haemagglutination (IHA) test 4. The diagnosis of HD can thus be established with the help of radiologic and serologic finding4. The diagnosis is also easier when the lesion has multiple locations involving different organs or when daughter cysts, germinal membrane detachment and calcification are present 2.

Surgery is the mainstay of treatment for hydatid cysts of the Liver. Laparotomy is the most common surgical approach6. Liver resection and pericystectomy are procedures that resect the closed cysts with a wide safety margin; however they are considered too radical procedures for hydatid cyst removal. Conservative procedures such as cystectomy and omentoplasty for hydatid disease should be the standard surgical procedure because of their safety, simplicity, and effectiveness in fulfilling the surgical treatment criteria of hydatid disease6. The peritoneal hydatidosis has also been successfully surgically removed with similar conservative procedures5, 7.

Symptomatic or large cysts should be surgically treated. In cases suspected of having peritoneal spillage, antihelminthic drugs should be administered8. In addition, small asymptomatic cysts, some daughter cysts, and peritoneal secondary cysts and splenic cysts may also be effectively treated with Albendazole8.


1. Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics 2000; 3:795-817.
2. Polat P, Kantarci M, Alper F, Suma S, Koruyucu MB, Okur A.: Hydatid Disease from Head to Toe. Radiographics 2003; 23:475-94.
3. Ammann RW, Eckert J. Cestodes. Echinococcus. Gastroenterol Clin North Am 1996; 3:655-89.
4. Husen YA, Nadeem N, Aslam F, Bhaila I. Primary splenic hydatid cyst: a case report with characteristic imaging appearance. J Pak Med Assoc 2005; 5:219-21
5. Karavias DD, Vagianos CE, Kakkos SK, Panagopoulos CM, Androulakis JA. : Peritoneal echinococcosis. World J Surg 1996; 20:337-40.
6. Buttenschoen K, Carli Buttenschoen D. Echinococcus granulosus infection: the challenge of surgical treatment. Langenbecks Arch Surg 2003; 4:218-30.
7. Hamamci EO, Besim H, Korkmaz A. Unusual locations of hydatid disease and surgical approach. ANZ J Surg 2004; 5:356-60
Balik AA, Celebi F, Basglu M, Oren D, Yildirgan I, Atamanalp SS. Intra-abdominal extrahepatic

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Scorpion stings are a common problem in many parts of the world often reported from rural areas in developing countries like India. Here we report 2 cases from a particular locality of Western Orissa, received in different clinical states and studied the effect of Prazosin , which is its first trial report from this Medical College.

Clinical , experimental and laboratory investigations have confirmed the inter-relationship between stimulatory effects of the scorpion venom on Autonomic Nervous System (A.N.S) and adrenals and subsequent effect of released transmitters on C.V.S. The envenomation due to Mesobuthus tamulus , an Indian Red Scoripion sting can result in an acute life threatening medical emergency. It has been reported that the severity of Scorpion sting depends upon the time between the sting and administation of Prazosin. Prazosin , an alpha adrenergic blocker acts as a physiological antidote to venom of Scorpion.

Scorpion sting, Prazosin, Autonomic storm, Pulmonary edema.

Case No. 1
A 32 year male admitted to Medicine – III unit on 24/09/2005 being bitten by an Indian Red Scorpion over right occipital area, 5 cm from mastoid process while sleeping over a Log of wood at around 9 P.M. After ½ hour of the bite he had blurring of vision, dryness of mouth, burning sensation over lips, with 2-4 bouts of vomiting. He was confused at that time and unable to identify his relatives, with urinary urgency and retention of urine. Then he was transferred to a local hospital and treated with injection Hydrocortisone Deriphylline, Nikethamide, IV fluids and Oxygen. As the condition deteriorated he was referred to V.S.S. Medical College Hospital , Burla.
There was no history of fever, convulsion and patient was not a known case of Diabetes Mellitus, HTN, PTB, Sickle Cell Disease. He was a farmer by profession with no addiction to smoking or alcohol.
At the time of admission patient was conscious, afebrile. On examination Pulse – 148/min., regular BP 90 mmHg, systolic (diastolic not recordable), respiratory rate 40/min regular, abdominothoracic type. There was pallor, central cyanosis. There was no edema, lymphadenopathy, JVP was not raised, skin was cold and clammy with features of dehydration. Chest examination revealed B/L, normal vesicular breath sounds with basal crepitations . Heart sounds were normal without any murmur, P/A revealed abdomen soft, non tender and no organomegaly, CNS examination was within normal limit. Local examination at the site of bite revealed no abnormality.
Hb% -9.8gm%,DC-N 84%, L 16%, M0, B0, E0, ESR-08mm 1st hour, TLC-29,500/mm3 of blood
RBS-138mg%, Serum Urea-42mg%, Serum creatinine-1.9mg%
Serum Ca++-7.7mg%,-Serum Mg+-1.6mg%
Uric Acid -6.0mg%
Serum Bilirubin -T(1.6mg%), D (0.4mg%)
S.G.O.T-42 I.U./L, S.G.P.T.-52 I.U./L,S. Alkaline Phosphatase: 120 I.U./L
Chest X-Ray:
Showed shaggy heart borders with features of pulmonary edema. Echo study showed normal LV function with global hypokinesia, decreased LV systolic function, mild M.R., mild TR without PAH.
Within normal limit in all 12 leads.
Patient was treated with injection Dopamine , Dobutamin, Deriphyline, Ceftriaxone, Odansetron, Ranitin and O2 inhalation. Patient did not show signs of improvement till 2nd day of treatment. On 3rd day Prazosin (2.5 mg/day orally) started in low dose. Patient started improving, BP increased gradually, chest became clear. Then on 5th day Prazosin was increased to 5 mg/day orally and patient improved rapidly. On 7th day patient became completely asymptomatic. Repeat chest X-ray and Echo were normal and finally discharged with advice to continue Prazosin for another 7 days.
After 15 days patient attended OPD for follow up. He was totally asymptomatic , lungs were clear, blood pressure and CVS examination were normal. Finally Prazosin was stopped.
Case No. 2
A patient aged 40 years, a resident of village about 4 kilometers distant from 1st case was admitted on 29/09/2005 being bitten by an Indian Red Scorpion on right 2nd toe at around 9:30 P.M. He suddenly developed severe pain without local reaction at the site of bite. After half an hour he developed 2 episodes of vomiting and profuse sweating and severe breathlessness. He was taken to a local hospital and treated with injection Dopamine, Deriphylline, I/V fluids, Steroid. When he lost his consciousness he was referred to this Hospital.
At the time of admission patient was confused with pallor, central cyanosis, dyspnoeic, with respiration rate – 48/min abdominothoracic regular, Pulse – 110/min regular , BP – 100/60 mmHg , cold and clammy extremities. Systemic examination revealed B/L Vesicular BS, coarse crepitations on lung bases associated with rhonchi. Heart sounds were normal without any murmur, CNS examination revealed patient was confused without any cranial nerve and motor involvement. Plantar reflex was normal and DTR normal without any meningeal signs.
Hb% -8gm%, DC-N 87%, L 13%, E0, M0, B0, ESR-08mm 1st hour, TLC-25,400/mm3 of blood
RBS-156mg%, Serum Urea-22mg%, Serum creatinine-1.6mg%
Serum Na+-123meq/lit, Serum K+-3.8meq/lit
Ca++-7.8mg%, Mg+-1.9mg%
Uric Acid -6.2mg%
Serum Bilirubin -T(1.4mg%), D (0.3mg%)
S.G.O.T-44 I.U/L, S.G.P.T-58 I.U/L, S. Alkaline Phosphatase: 130I.U./L
Chest X-Ray: Within normal limit
ECG: Within normal limit in all 12 leads
Patient was treated with Tablet Prazosin 5mg injection Dopamin, Dobutamine, Deriphyline, Cefriaxone, Odansetron, Ranitin, O2 inhalation. Patient responded dramatically. On 3rd day he became asymptomatic with normal BP. Lungs became clear. Patient was stable on 5th day with normal vital signs and finally discharged on 4/10/2005.
Patient was followed up after one week. He was completely normal and Prazosin was stopped.
Indian Red Scorpion sting can present as an acute life threatening medical emergency often reported from rural areas. The sting frequently occurs at night because of Scorpion’s nocturnal habit.
Scorpion sting activates sodium neuronal channels causing excessive neuronal discharge.
The severity of Scorpion stings depends on patients age, season, the time between the sting and treatment with Prazosin. The signs and symptoms are due to potent autonomic storm in victims characterized by transient cholinergic effects1 – profuse sweating – hypersalivation, priapism in males, hypotension, bradycardia, ventricular ectopics and prolonged adrenergic effects – hypertension, tachycardia, cool extremities and pulmonary oedema. Vomiting , sweating, priapism and cool extremities are early diagnostic features of M. tamulus envenomation.
Pulmonary edema in Scorpion stings is of haemodynamic origin and related to a severe and prominent impairment of left ventricular systolic function.
Alpha receptor stimulation plays an important role in pathogenesis of Scorpion stings. Prazosin, an adrenergic alpha –1 blocker (invented in 1983-84) possesses pharmacologic properties that render it most suitable in antagonizing the toxic effect of Scorpion venom.
Prazosin reduces the pre-load and left ventricular impedance without rise in heart rate and rennin secretion3. It decreases pre-load and therefore causes no increase in cardiac output and heart rate contrast to hydralazine. It counters the action of local tissue liberated angiotensin – 2 in myocardium and also counters the vasoconstriction induced by liberated endothelin due to catecholamine excess by enhancing Nitric Oxide as a result of accumulation of C-GMP in vascular tissues by inhibiting phosphodiesterase. Scorpion venom inhibits insulin secretion which is counter acted by Prazosin.
Usual dosages2 is 250 mcg in children and 500 mcg in adults given to those having signs and symptoms of sever Scorpion sting irrespective of blood pressure provided there is no signs of hypovolemia.
From the above case report studies it was concluded that Prazosin reverses blood pressure, pulmonary edema irrespective of blood pressure and acts as a physiological antidote to scorpion venom.
1. Symptoms , Signs and Management of Indian Red Scorpion Envenomation – H.S. Bawasar , P.H Bawasar, Medicine Update , Vol No. 8, 1998, P 752 – 753.
2. Harrison’s Principle of Internal Medicine, Vol II, 16th Edition, P. 2604.
3. Bawasar H.S, Bawasar P.H., Prazosin in the management of Cardiovascular manifestation of scorpion sting – Lancet, 1986, P 510- 511.

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Organophosphorus induced delayed neuropathy (OPIDN) is a delayed sequel of organophosphorus poisoning, occurs rarely1,2,6 after an acute cholinergic crisis and is confused with Guillain Barre’ Syndrome (GBS) or other causes of polyneuropathy. We report one case of OPIDN which we managed conservatively with steroids & we found improvement of CMAP (Compound Muscle Action Potential) within one month.

Organophosphorus (OP), OPIDN, Axonal degeneration, neuropathic target esterase (NTE), Pralidoxim (PAM).

OPIDN refers to delayed effects of organophosphorus poisoning (OP poisoning), occurs due to binding of esterase enzyme called neuropathic target esterase (NTE)2,3 and cause predominant axonal degeneration (dying back axonopathy5) and minor demylenation7. Typically patient presents 3-5 weeks after OP poisoning with lower extremity weakness, bilateral foot drop, glove and stocking type of sensory loss5. Present case study documents one case of OPIDN due to tri Ortho cresyl phosphate poisoning after one month of cholinergic crisis and prevention of OPIDN is by early treatment of cholinergic crisis with PAM (before organophosphorus compound ages), steroids and other supportive measures (e.g splintage, physiotherapy and carbamazepine for neuropathic pain).

A 19 year male presented to the hospital with complains of tingling sensation and weakness of lower limbs and hands 15 days back. He was apparently alright 15 days back, had 4 episodes of loose motion which subsided with medication. Then he had tingling sensation over lower limbs and hands and weakness of lower limbs followed by weakness and clumsiness of both hands. Weakness was progressive and in one week the patient was not able to walk. No history of fever, dog bite, vaccination, previous similar episode, contact, diabetes, leprosy was elicited.

Allegedly he took insecticides and suffered from acute cholincrgic crisis one and half month ago for which he was hospitalized for 11 days and recovered. On general examination the patient was conscious, afebrile with pulse rate 80/min, BP 126/80mm Hg without any other positive findings. CNS examination revealed intact cranial nerves, wasting of hypothenar, thenar (Fig. 1), calf and peroneal muscles of limbs (Fig. 2). Hypotonia involving flexor and extensor of ankle, weakness of abductor pollicis berevis, adductor pollicis and oppones pollicis seen. Long flexors and extensors of digits were normal. Lower limbs evertor, invertor, flexor and extensor of ankle were 0/5 power on both sides. Extensor and flexor of knee and hip were normal. Supinator jerk was diminished, ankle jerk was absent on both sides. Rest deep tendon jerks were normal. Plantar was nonresponsive both sides. There was in-coordinated movement, Rhomberg's test was positive and gait was high stepping. Sensory examination revealed all modalities diminished below ankle and wrist bilaterally. Peripheral nerves were normal.

Laboratory investigation revealed:
o Hb 12.7 gm%, TLC 10,700/mm3, DC N-69 L-30 E-l, ESR 8mm/lst hr, FBS 85 mg% .
o Serum Na'-132meq/lt, Serum K-4.8meq/lt, Serum urea -28mg%, Serum creatinine -1.18 mg%.
o HIV ELISA - Negative, CSF study showed TLC 3/mm3 (all lymphocytes) RBC absent, Glucose 61mg%, Protein 27 mg%, TB ELlSA- Negative.

Initial Nerve Conduction Study:
Motor - Compound muscle action potential (CMAP) was absent in bilateral Median, Common peroneal nerve (CPN) , bilateral posterior tibial nerve (PTN).
CMAP in bilateral ULNAR - Amplitude less than normal, velocity in right ulnar less than normal , Left ulnar velocity within the normal limits.
Sensory - In bilateral Median Velocity was reduced, Right ulnar velocity was reduced no potential in Right sural, left Sural velocity and amplitude within normal limit.

Repeat Nerve conduction Study: (After one month)
CMAP- left median no potential, Right median small amplitude potential
Velocity in the above is reduced
Conduction in bilateral ulnar as before
No CMAP in bilateral CPN and bilateral PTN
Sensory as before

Chronic complication of OP poisoning are neurobehavioral and poly-neuropathy1. Sensory motor polyneuropathy or OPIDN typically ocours after 3 to 5 weeks of exposure where motor deficit dominates the clinical picture5. Patient initially complains of tingling sensation over extremities, symmetric lower extremity weakness, and leg cramping and calf pain. Atrophy of calf muscles, ataxia and bilateral foot drop gradually ensues. It may progress to cause truncal weakness. Cranial nerves and autonomic system are not involved3. Sensory symptoms resolve over months. In mild cases motor symptoms may resolve over 15 months or may not resolve at all3. Severe cases may develop spasticity due to spinal cord involvement in the form of diffused spinal cord atrophy predominantly of thoracic spine2,5. Neuropathology of OPIDN demonstrates that large distal neurons tend to be affected first. There is slowing and stoppage of axonal flow, blockage transport of protein and other substances as well as demyelination7. Axonal degeneration precedes demyelination and there is "dying back" axonopathy5. Site of OP attack is a membrane bound target esterase called neuropathic target esterase (NTE)2,3. Function of NTE is not known. It is present in brain, spinal cord and peripheral nerve6, lymphocytes4 where specific OP binds and ages1 by losing 1 carbon and forming P-O carbon linkage. Critical mass of 70% of NTE must be inhibited to cause clinical symptom6. The delay in symptoms is due to the fact that not all axons will degenerate at the same time and nerve may continue to function until significant number of axons is degenerated.

OPIDN diagnosis is made by clinical and neurophysiologic examination and ruling out other possibilities. Currently platelet, RBC and lymphocyte NTE inhibition for confirming neuropathic potential of organophosphorus is under study . Use of hen test as screening test of neurotoxicity is flawed1.

Treatment of OPIDN is conservative and can be prevented by early and prolonged use of PAM. Tingling sensation over palm and sole responds to carbamazepine5.

1. Angelo Moretto et al: Poisoning by organophosphorus insecticides and sensory neuropathy; J. Neurol. Neurosurg. Psychiatry: 1998;64;463-468.
2. Cnia-Chang Chuang et al: Delayed Neuropathy and Myelopathy after Organophosphate Intoxication: NEJM, Volume 347:1119-1121 October 3, 2002 Number 14.
3. J. Mirandal et al : Muscular Strength and vibration thresholds during two years after acute poisoning with organophosphate insecticides. Occupational and Environmental Medicine BMJ 2004; 61: e4.
4. M. Lotti et al: Inhibition of lymphocyte neuropathy target esterase predicts the development organophosphate induced delayed polyneuropathy:J. Arch of Toxicology, Vol 59/3 Oct 1986, Pg 176-179.
5. R. Hierons and M.K. Johnson : Clinical and Toxicological investigations of a case of delayed neuropathy in man after acute poisoning by an organophosphorus pesticide: J Arch of Toxicology, Issue Volume 40, Number 4/Deceber , 1978.
6. Singh H, Sharma N: Neurological Syndromes Following organo-phosphate poisoning, Year 2000 , Neurology India, Volume 48, issue 4, Page 308-13.
7. Versik P et al: Chronic Toxic Neurophaty in Qualis: British Lek Letsy 106 (10), 293 – 296, 2005.

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Acute Inflammatory Demyelinating Polyneuropathy following Malaria is a rare clinical presentation. Few cases have been reported so far from India and abroad. Here we report such a case from this hospital and discuss the pathophysiology and management.

Acute inflammatory demyelinating polyneuropathy (AIDP),
Plasmodium falciparum,
IV immunoglobulin.

Acute inflammatory demyelinating polyneuropathy (AIDP) is acute, frequently severe and fulminant which is auto immune in nature characterized by rapidly developing areflexic ascending motor paralysis with or without sensory disturbances. 75% of cases are preceded 1-3 weeks by an acute infectious process usually respiratory or gastrointestinal. The reported microorganisms include Campylobacter jejuni, Mycoplasma, Human herpesvirus, CMV, E-B virus etc3. The AIDP following malaria is of rare occurrence. However recently several cases have been reported following both vivax and falciparum malaria1,5.

A 16 years boy from sonepur was admitted to this hospital on 18.06.2006 with complains of sudden weakness of both lower limbs and both upper limbs and inability to walk for 10 days. Twelve days back he had fever with chill and rigor for which he consulted local physicians and detected to be a case of Falciparum Malaria (slide +ve) and treated with chloroquine tablets. Next morning the patient noticed weakness and tingling sensation of both lower limbs. He was treated with IV fluids and multivitamin injection. The weakness rapidly progressed and after 2 days he developed weakness of both upper limbs and paralysis of both lower limbs leading to inability to walk. He was treated at the District Hospital with antimalarial drugs and referred to this Hospital.

On admission the patient was febrile (Temp. 99.80 F) conscious. There was mild pallor without icterus, clubbing, cyanosis, oedema or Thyroid enlargement. Pulse was 96/min, regular, B.P. was 120/80mm of Hg in both upper limbs. Respiration rate was 16/min. and abdominothoracic type. There was no sign of dehydration.

Neurological examination revealed normal higher intellectual functions with all cranial nerves intact without any pupillary abnormality. Motor examination showed normal bulk and tone of all muscles in upper and lower limbs. Power in both upper limbs were 3/5 grade in proximal groups and 4/5 grade in distal groups including hand grip weakness. Power in both lower limbs were 2/5 grade in proximal group (flexor, extensor around hip) and grade 3/5 around knee, ankle and feet. Power in trunk muscle and abdominal muscles were normal. Bladder and bowel were not involved. Coordination could not be tested and there was no involuntary movement. Deep Tendon reflexes in all four limbs were absent. Plantar was non responsive in both limbs. All the superficial reflexes were absent. Gait and Romberg’s test could not be done due to weakness. Sensory system examination showed all modalities intact. Autonomic nervous system was normal. Skull and spine was normal without any sign of meningitis.

Respiratory system, cardiovascular system, gastrointestinal system and other systems were normal.

There was no such past history. There was no history of SCD, TB, DM, HTN, exanthematous fever or dog bite. Family history was not suggestive.

Routine examination findings were-
HB – 9gm% ,TLC – 10,200/mm3, DC – N-64, L-30, E-6, M-0, B-0, ESR – 46mm 1st hour
ICT for Malaria – PFR ++
Serum – Na+ - 138m Eq/l, K+ - 4.2m Eq/l, Ca+ - 8mg%
Serum urea – 46mg%
Creatinine 1.5mg%

LFT – Serum Bilirubin – 1.3mg%(Total), 0.4mg% (Direct), SGOT- 42 IU/L, SGPT-97IU/L, Alkaline Phosphatase - 548IU/L. Chest X-ray PA view and X-ray of Lumbosacral spine were normal . Ultrasonogram of abdomen and pelvis was normal. CSF was clear with normal pressure, CSF cell count was 12/ml mostly lymphocytes, Glucose was 58mg%, protein 240mg% and gram stain and AFB were negative. Nerve conduction studies in both median, ulnar and common peroneal nerves revealed gross reduction in amplitude and motor nerve conduction velocity. The distal latency was grossly prolonged in all the nerves. F waves were absent in all the nerves. The sensory conduction in both median and common peroneal nerves was absent.

The patient was diagnosed to be a case of AIDP fllowing falciparum malaria. He was treated with full course of injection Artesunate and IV immunoglobulin 20g/day for 5 days. The patient improved after 3 days of completion of immunoglobulin . The power in all four limbs improved. On 10th day of admission the patient was discharged with follow up advise.

Acute inflammatory demyelinating polyneuropathy (AIDP) are seen following viral, bacterial infections or immunization and is uncommon following parasitic infection like malaria2. It is important to rule out other neurological syndromes that may be unmasked by febrile episode.

The pathogenesis of AIDP following malaria is not known. This is likely to be immunogenic that occurs after viral/bacterial infections.

Other possible mechanisms suggesting development of polyneuropathy following a parasitic infestation include:
• Parasitic emboli obstructing vasa nervosum.
• Release of neurotoxins.
• Associated metabolic and nutritional disturbances.
• Immune mediated capillary damage.
• Release of free radicals and tumors necrosis factor.

AIDP is a variant of GBS manifests as rapidly developing areflexic motor paralysis with or without sensory disturbances. The pattern is ascending type and first noticed as rubbery legs. Weakness typically evolves over hours to few days and frequently associated with tingling dysesthesia in extremities.

Legs are affected more than arms. All the reflexes are absent. Lower cranial nerves are frequently involved. Bladder involvement is rare. In severe cases autonomic dysfunction may occur, resulting in fluctuation of blood pressure, postural hypotension, cardiac dysrythmias.

Modified A.K. Asbury Criteria (for GBS):
Required Criteria:
• Progressive weakness of 2 or more limbs due to neuropathy
• Areflexia
• Disease course < 4 weeks
• Exclusion of other causes like vasculitis, botulism, diphtheria, porphyria, cauda equina syndrome.
Supportive Criteria:
• Relatively symmetric weakness
• Mild sensory involvement
• Facial or other cranial nerve involvement
• Absence of fever
• Typical CSF profile (Acellular , Increase protein level)
• Electrophysiological evidence of demyelination

Treatment is to be given as early as possible. In > 2 weeks of first motor symptoms, immunoglobulin is not effective. IVIg is administered as five daily injections for a total dose of 2g/kg body weight.

A course of plasmapheresis consisting of 40 to 50ml/kg, plasma exchange four times a week is usually employed. Combination has no advantage. Steroid has no role. In worsening phase critical care and ventilatory support is required.


In conclusion we report that falciparum malaria may present as AIDP and this possibility though uncommon must be taken into consideration while encountering patients in endemic areas.

1. Kanjalkar M, Karnad DR, Namayan RV, Shah PU: Guillain-Barre Syndrome following malaria, J. Infect 1999; 38: 48-50.
2. Sokrab RT, Eltahir A, Idris MN, Hamid M: GBS following acute falciaprum malaria, Neurology 2002, OCT, 22; 59(8), 1281-3.
3. Harrison’s Principle of Internal Medicine, 16th Edition, Vol – II, ; 365: P2513-14.
4. Corner DH, Herber JM, Parasitic infections of the pripheral nervous system in: Dyck PJ, Thomas PK, eds. Peripheral neuropathy, Philadelphia: WB Saunders; 1993 PP. 1338 – 90.
Chakravarty A, Ghosh B, Bhattacharyya R, Sengupta S, Mukherjee S: AIDS following

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Delayed cerebellar ataxia is a rare acute self limiting complication of falciparum malaria [2]. This complication is predominantly found in Sri Lanka though few cases have been reported from India and Africa [2,4]. We have recently encountered such a patient in our hospital. The case is described below with pertinent literatures reviewed.

Delayed cerebellar ataxia, Plasmodium falciparum

Delayed cerebellar ataxia found in falciparum malaria is usually an acute self limiting and isolated ataxia without cerebral involvement [4]. The patient usually shows features of midline cerebellar involvement and is characterized by cerebellar gait and truncal ataxia [1,4]. Most of the patients are afebrile before the onset of symptoms [1,4].

A 45 year old engineer was admitted to the hospital in September '07 with complaints of difficulty in maintaining balance with a tendency to fall in all directions for the past four days. He developed high grade fever, intermittent in nature associated with chills and rigor and subsided with profuse sweating. He was admitted in the local hospital and was detected having falciparum malaria by MP slide and was treated with anti-malarials and antibiotics. The patient became afebrile after five days and was discharged. Four days later He developed instability of gait such that he lurched and fell in all directions – this left him unable to walk. He was then referred to our hospital for further investigations and management.
There was no history of diabetes mellitus, hypertension, tuberculosis or sickle cell disease.

Family history is also not suggestive of diabetes mellitus, hypertension, tuberculosis or sickle cell disease.

On admission the patient was found to be conscious afebrile. There was mild pallor, no cyanosis, icterus, clubbing, edema, Lymph node or thyroid enlargement, JVP was not raised, Pulse was 80/ min regular, B.P. 150/ 84 mm of Hg, Respiratory rate of 18/ min and temperature was 36.4 ° C.

Neurological examination revealed normal higher mental function. All cranial nerves were found normal. Motor system examination revealed normal bulk, tone and power. The gait was broad based with irregular stepping and a tendency to fall in all direction. No sensory impairment or autonomic involvement was found. On finger nose testing revealed past pointing; the knee heel shin test was found to be clumsy bilaterally. Disdiadochokinesia was present bilaterally. The deep tendon reflexes were normal, plantar was bilaterally flexor. The cranium and spine was normal and there were no signs of meningeal irritation.

The respiratory, cardiovascular, and gastrointestinal system was found to be normal.

On investigation Hb% was 11.2 gm/dl, DC N72 E3 L25; Total leukocyte count was 7100/cmm and ESR was 6 mm in 1st hr. Routine blood biochemistry  Fasting blood glucose 110 mg/dl, urea 28 mg/dl, creatinine 1.4 mg/dl, serum Na+ 147mEq/l and K+ 4.0 mEq/l. Malaria parasite by ICT was found to be positive. CT scan of brain was found to be normal and no abnormality was detected by pure tone audiometry bilaterally. CSF study was found to be normal.
The patient was diagnosed as having delayed cerebellar ataxia following falciparum malaria. He was treated with a full course of inj. Artesunate for 5 days. The patient rapidly improved and by the 5th day he was able to walk on his own. The cerebellar signs disappeared on the 6th day and he was discharged with advice after 7 days of admission.

Neurologic features found in malaria are usually not consistent; the commonest being altered sensorium followed by seizures [1]. But cerebellar involvement is the most consistent neurological manifestation of complicated as well as uncomplicated malaria as Purkinje cells are susceptible to damage due to hyperpyrexia [4].

RBCs with parasitized P. falciparum adhere to the endothelial wall of capillaries in a certain phase of its cycle. Parasites derive some nutrition from endothelium. This phenomenon occurs maximally in the capillaries of brain [1]. Focal hemorrhage or non hemorrhagic infarcts in cortex, basal ganglia, thalamus, pons and cerebellum have all been described in cerebral malaria [1]. Immunologic mechanism, as a cause for delayed cerebellar ataxia has been postulated; cerebellar demyelination following falciparum malaria has been reported in several patients from Sri Lanka and India occurring several days after recovery [1,4]. The CT scan of brain is normal [1,2]. The disease has an excellent prognosis with complete recovery in 3 months [2,4]. The patients are treated symptomatically though some physicians prefer to use steroids.

Cerebellar involvement in falciparum malaria may be due to selective clogging of cerebellar micro vasculatures with parasitized RBCs, perivascular hemorrhage, microscopic infarcts, shrinkage of purkinje cells and perivascular clusters of microglia, carrying a high mortality rate [1,3] or, may be due to immunologic mechanism as in the case of delayed cerebellar ataxia [1,4].

Delayed cerebellar ataxia is a rare complication of cerebellar involvement following falciparum malaria and may be considered in the differential diagnosis in patients showing cerebellar signs especially if the patient gives a past history of fever. This is the first reported case of delayed cerebellar ataxia from our institution.

1. Adult cerebral malaria: prognostic importance of Imaging findings and correlation with postmortem findings; Tufail F. Patankar, MD, Dilip R. Karnad, MD, Prashant G. Shetty, MD, Anand P. Desai, MD, Srinivasa R. Prasad, MD;Radiology 2002;224:811-816
2. Delayed cerebellar ataxia following Falciparum malaria: Hussam Alsoub, MD : Annals of Saudi Medicine,1999;Vol 19, no. 2: 128-129
3. MR of cerebral malaria; Yves Sébastien Cordoliani, Jean-Luc Sarrazin, Dominique Felten, Eric Caumes, Cristophe Lévêque, Alain Fisch; AJNR Am Neuroradiol 19:871-874, May 1998

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Neurocysticercosis is most common parasitic infestation of CNS1. The incidence of spinal involvement is 1.5-3%4.Spinal neurocysticercosis usually appear due to mass effect. Most cases occur in subarachnoid space but intra medullary location is extremely rare1. Here we report a case of intramedullary neurocysticercosis (reported about 50 cases sofar) 4 and discuss the disease.


Neurocysticercosis (NCC), Spinal neurocysticercosis (SNCC), intra medullary, Tinea Solium, MRI.

A 26 year named BC , from Salepur presented to this hospital in June 2008 with c/o of head ache & neck pain(1 month), numbness of right side of face(15 days),inability to hold objects properly in right hand (15days).He was alright 1 month back. Started with continuous headache relieved with analgesics, without associated vomiting, nasal stuffiness or blurring of vision. After 15 days he developed numbness of right side of face & noticed weakness of right hand which gradually progressed so that he could not hold any object properly. There was no history of fever, root pain, or convulsion. There was no bladder or bowel involvement. There was no h/o Diabetes, trauma, hypertension or tuberculosis. Family history was not suggestive. He was not habituated to alcohol or smoking. There was no contact history& he was unmarried.
On examination he was of average built having BP- 130/80 mm of Hg; pulse 68/ min, regular; without pallor, jaundice or lymphadenopathy.
CNS examination revealed patient to be conscious with normal higher functions including speech. All the cranial nerves were intact except diminished pain sensation on right side of face. Motor system showed normal bulk with increased tone of muscles in legs & arms. Power was grade V in both lower limbs but grade IV in both upper limbs. Hand grip was weak on both sides, right >left. Bicep & triceps reflexes were exaggerated on both sides with normal supinators. Knee & ankle jerks on both sides were exaggerated. Plantar was extensor on right but flexor on left. Sensory system was normal. Skull & spine was normal without any meningeal or cerebellar signs. Fundus was normal.
Other systems like CVS, GIT, respiratory did not reveal any abnormalities.
Routine investigations like Hb%, DC, TLC, FBS, urea, creatinine serum K+, Na+ were normal. ESR was 25/1st hour & Mx was negative. Chest X-ray & cervical spine X’ray were normal. CSF study was normal. MRI of brain & spinal cord showed ring enhancing tiny lesions at cervico medullary junction inside the medullary central canal with consequent syrinx formation..(Figure-1,Figure-2) Anticystocercal antibody was positive.
A young male presenting with gradual onset of assymetrical weakness of upper & lower limbs, with headache & diminished pain sensation of right side of face without significant involvement of lower limbs with features of UMN involvement in the form of hypertonia & hyper reflexia of all limbs below C4 without sensory level a provisional diagnosis of high cervical cord compression ( intramedullary) was thought of, probably involving trigeminothalamic tract(right) & corticospinal tract below pyramid (right). With the investigations the patient was diagnosed as a case of SNCC with obstructive syringomyelia.
The patient was treated with Albendazole 400 mg twice daily for 28 days with oral prednisolone in tapering dose.In the next followup after one month he complained of progressive weakness of upper limbs with no response to Albendazole.Hence he was advised for neurosurgical consultation for excision of the cyst.
Neurocysticerosis is the most common parasitic infestation of CNS caused by ingestion of eggs of Taenia Solium3.T.Solium has its definite host in human being where adult worm stays in intestine laying eggs which are taken by pigs who are intermediate hosts. The embryo cross the intestine and reside in CNS, muscles, eyes and skin as cysticerci.Human beings have the disease when they ingest the eggs instead of Pigs. The eggs hatch in the intestine and develop into cysticerci in the above mentioned organs.

Usual organs involved in Neurocysticerosis are brain, eye, subcutaneous tissues.Common presentation of cysticerosis of brain are headache, seizure and focal neurological deficit.

Spinal neurocysticerosis is a rare presentation; the incidence ranging from 0.7-5.85%1,3.Spinal forms have been identified in vertebral, extradural, intradural, intramedullary regions.Intramedullary cysticerosis is very uncommon1. Migration of the cysticercus through the ventriculo-ependyal pathway and haematogeneous dissemination has been identified as pathogenic mechanism1,4.

In absence of previous history or subcutaneous nodule it may be difficult to suspect clinically intramedullary cysticerosis.High eosinophil count with soft tissue calcification though suggestive is rare.Result of surgery has not been encouraging due to parenchymal gliosis as a result of toxic waste from larva, pachymeningitis and vascular insufficiency.
But in the era of microsurgery good outcome has been reported. Medical treatment of intramedullary lesions can be considered in patients of stable neurological status but impossible in acute or progressive cases.Post operative anticerceal drugs should be given as it is a generalized disease with focal manifestation1.
SNCC is rare compared to intracranial as cysticerci do not pass through subarachnoid space at cervical level due to its size(sieve effect).Besides CSF reflux at craniovertebral junction propels floating cysts back into intracranial space than spinal canal.

Several possible mechanisms of spinal invasion are:-
(a)Ventricular cysticerci pass through Magendie or Luschka foramen, migrate by gravity through subarachnoid space to inoculate spinal cord commonly cervical region.
(b)Haematogeneous spread explain intramedullary lesion,commonly thoracic area due to increased blood flow.(c) Intraventricular hypertension enables migration through a dilated ependymal canal into spinal cord explaining intramedullary invasion.Other favorable conditions favoring spinal invasion may be due to NCC-related hydrocephalus and/or meningitis, use of antiepileptic drugs like Carbamazepine or Phenytoin which can after immune function leading to parasitic infestation3.

The location of mass lesion, its size, the inflammatory response generated by cyst breakdown are important factors for management.Brain blood flow is 100fold greater than spinal explaining more intraventricular lesion.In spinal form thoracic region having more blood flow explains high incidence.The location of cysticerci is cervical - 34%,thoracic -44.5%, lumbar -15.5% and sacral- 6%.MRI is the investigation of choice.
Concurrent intracranial lesion are seen in spinal involvement. As long as cysticercus is viable there is relative host immune tolerance. Massive antigen response occurs with death of parasite with intensification of immune/inflammatory response.Surgery is required for diagnosis and treatment though outcome is mixed. Albendazole or Praziquantel with or without steroid are used. Albendazole is preferred as blood level are increased with steroid.Spinal intramedullary cysticercosis represents a challenge for diagnosis & surgery. Patient recovery is variable. Despite promising reports the safety and efficacy of medical treatment remains unproved4.

1. Singh P, Sahai K.-Intramedullary cysticercosis.Neurol India 2004;52:264-5
2. Mohanty A.Venkatrama SK, Das BS,Rao BR,Vasudev MK -Spinal Intramedullary cysticercosis-Neurosurgery.1997; Jan 40(1):82-7
3.Dong Ah Shin & Hyun Chul Shin-Yonsei Med.J.2009,Aug 31;50(4):582-584.
A case of extensive spinal cysticercosis involving whole spinal canal with a h/o cerebral cysticercosis.
4.Agarwal R,Chauhan SPS, Mishra V, Singh PA,Gopal NN-Acta biomed 2008;79,39-41
Focal spinal intramedullary cysticercosis.

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Primary 1. Association of serum Ca++, Mg++ level in cases of hypokalemic disorder.
Secondary 2. Response of treatment with potassium supplementation and Mg++ and Ca++ requirement.

Fifty cases of hypokalemia, most of them having history of hypokalemic periodic palsy, were taken for study, in department of medicine for November 2003 to April 2005. Detail clinical history, physical examinations and routine laboratory investigations done including mandatory serum Na+, K+, Ca++, Mg++. The laboratory investigation of serum electrolytes were repeated after 2-3 days of K+ supplementation and in resistant hypokalemic cases with magnesium deficiency, Mg++ supplementation was given first and then Ca++ supplementation in combined Ca++ deficiency cases.

Out of the 50 patients, 25% were males (30-60 years), 40% were females 18-40 years. Commonest presentation were paraplegia (75%), Quadriplegia (25%), vomiting (20%), Hicough (4%), Tetany (2%), Bradycardia (6%), Paralytic ileus (2%) and various ECG changes ie. U wave, increased PR interval, decreased T wave etc. Most of the patients belonged to low socio-economic status and most of them were physical labourers. In moderate to severe hypokalemia, hypomagnesemia was commonly present ( 64%) and hypocalcaemia (28%). Most of these cases responded to K+ supplementation but in some cases with severe hypokalemia associated with hypomagnesemia and hypocalcaemia were resistant to K+ supplementation. In these cases long with K+ , Mg+ supplementation was given, after which patients responded rapidly and satisfactorily. Dramatic improvement was seen in the power of limbs after supplementation of K+. However n 6% patients no significant improvement was seen after 2-3 days and Mg+ was supplemented orally after which there was improvement in power of limbs and serum K+ level rapidly.
Hypokalemia Hypomagnesemia Hypocalcemia
Mild (3.0-3.5 meq/l) 3(6%) 0(0%)
Moderate (2.5 – 3.0 meq/l) 7(14%) 6(12%)
Severe(<2.5 meq/l) 22(44%) 8(16%)

(Incidence of Hypomagnesemia and hypocalcemia according to severity of hypokalemia)

It was observed that in hypokalemic disorders there is derangement of other electrolytes (i.e Serum , Mg++, Ca++). In moderate to severe hypokalemia estimation of serum Mg++ and Ca++ is mandatory and Mg++ replacement should be done after K+ supplementation and before Ca++ supplementation in combined electrolyte disorders to avoid arrythmia.

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