THYROID HORMONE STATUS IN ACUTE MYOCARDIAL INFARCTION
Posted by on Thursday, 22nd July 2010
1.
The thyroid is one of the important endocrine glands in human being. It secretes hormones like thyroxine (T4), tri –iodothyroine (T3) and calcitonin. The relationship between the thyroid gland and various body functions was studied in 1827 (Werner & Ingbar). Perry in 1835 described the clinical manifestation of exophthalmic goiter. Its association with angina pectoris and congestive heart failure.
In peripheral tissues,T4 in mainly metabolized to form active hormone 3,5,3’ – triiodothyronine (T3) and inactive 3,3’,5’,- triiodothyronine (reverse T3) as per the demand of the body (Bitman et al, 1971 and Chopra et al 1978). Non – thyroidal acute and chronic illnesses are the major cause of disordered peripheral thyroid hormone metabolism often poses a major problem in interpreting thyroid function tests (Cavalieri and Repport. 1971) it is generally agreed that despite gross abnormality in circulating thyroid hormones, most of these ill patients are clinically euthyroid.
A wide variety of systemic illnesses like infarction. malignant disease, hepato –cellular failure, renal failure protein – calorie malnutrition, congestive heart failure are associated with decreased T3, elevated reverse T3(rT3) and decreased, normal or increased serum T4 concentration. (Burger et al 1976, Rosenthal and Cavelieri, 1979).
AMI, frequently fatal form of ischemic heart disease (IHD) results due to considerable jeopardisation of coronary blood flow, is one of the commonest systemic nonthyroidal illnesses where thyroid hormone economy in altered. But conflicting reports regarding thyroid status has been published in this condition. Supra normal value of T4 in AMI have been observed by Wierainga et al 1981, Vanhaelst et al 1976 and Kirkeby et al 1984.
On the other hand decreased T3 and T4 in face of elevated reverse T3 has been observed by Kaplan 1977, Westgreen et al 1977 and Marek et al 1980.
Normal T4 with unequivocal elevation of rT3 and significant reduction of T3 also have been found by Smith et al 1978, Fabre et al 1980 and Lada et al 1981.
It has been also observed that magnitude of lowering of T3 and T4 correlates well with the severity of illnesses and survival. (Larty et al 1975 and Kaptain et al 1978, 1982)
The outcome of AMI depends of many factor like degree of myocardial damage, associated arrythmias, hypotension and shock.(Hurst 1982). How ever, commonly sudden death occurs in those cases with or without complication.
It is the intended:-
1. To study the thyroid hormone levels in AMI through out the illness.
2. To correlate the changes of thyroid hormone levels with the severity of these conditions.
3. To correlate the thyroid hormone levels with outcome that is recovery or death.
The thyroid is the largest endocrine gland. In the past it escaped the notice of most of the investigators owing to its inconspicuous shape and position. Vasalius in 1543 described it in details while Whartsen in 1656 named the organ “The Thyroid”
The relationship between the thyroid gland and various body function was studied in 1827. Parry in 1835 described the clinical manifestations of exophthalmic goiter and its associations with angina pectoris and congestive heart failure. In 1915 Kendall found the L – thyroxine (T4) from thyroid tissue whereas Pitterson and Gross found tri – iodothyronine in plasma and thyroid in 1954. ( Werner and lngbars H.,1971). Several studies have shown the relationship of the thyroid hormones with the thyroid and non thyroidal illnesses ( Herrison, Mc Donald, Hoffman, and Pool). Levy in 1971 demonstrated increased adrenergic activities in hyperthyroidism.
The Thyroid is highly vascular and comprises the follicles which contain proteinacious colloid. The colloid contains glycoprotein, thyroglobulin (TG) within which thyroxine(T4) and Tri – iodothyronine (T3) are formed and stored. Moreover, thyroid contains parafollicular cells which secrets calcitonim. (Copp & Co- workers in 1962).
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PSEUDOXANTHOMA ELASTICUM PRESENTING AS HAEMATURIA – A CASE REPORT
Posted by on Thursday, 22nd July 2010
1.
ABSTRACT:
Pseudoxanthoma elasticum is a rare inherited disorder of connective tissue, characterized by general elastorrhexis of the elastic tissue in the dermis, the blood vessels and Bruch membranes of the eye.
KEYWORDS:
Pseudoxanthoma elasticum (PXE), Angioid streaks, Bruch’s membrane, Connective tissue, Haematuria.
CASE REPORT:
A 55 years Hindu female presented with complain of recurrent haematuria for 6 months, diminished vision for one year and weakness of left half of the body since 3 years. She had attended menopause and was under Enalapril (5 mg) since 1 year for hypertension. No history of diabetes, tuberculosis or CAD. No suggestive family history.
On examination the patient was of average built with BP 130/80mmHg (both upper limbs) , pulse rate 80/min, regular (Brachial) good volume while diminished pulsation of both radial, ulnar, posterior tibial and dorsalispedis arteries. Both carotids, axillary, femoral and popliteal artery pulsations were well felt. She was mild anaemic without icterus, cyanosis, clubbing or lymphadenopathy. JVP was not raised. Thyroid was normal. Chest examination revealed vesicular breath sounds without any added sounds. Cardiovascular system examination revealed normal apex with normal heart sounds, without any murmur. P/A examination was normal without any renal brui. On CNS examination the cranial nerves, motor, sensory systems were normal without any cerebellar signs or meningeal signs. On examination of the skin, there were laxed skin with yellowish Xanthomatous lesions over neck and upper chest (Fig. 1, 2). Eye examination revealed vision 6/9 (Lt) and 6/6(Rt) and fundoscopy showed macular choroiditis with angioid streaks on left side (Fig. 3).
Routine Investigation Showed: FBS - 82mg%, PPBS – 104mg%, Blood Urea 20 mg%, Serum Creatinine 1.08mg%, ESR - 20mm/1 hour, DC N72, L25, E3, M0, B0, and TLC - 8000/mm3, Lipid Profile of serum were Sr. Total cholesterol -160mg%, TGS -108mg%, HDLC -48mg%, LDLC- 92mg% and VLDL-C -21mg%, Urine analysis showed proteinuria(+) and 10-15 RBC/HPF and RBC casts. Mantoux test was 18mm , ECG was normal.
ECHO Showed: Mitral value thickened, EF – 65%, Aorta – 32 mm, MACS – 17 mm, LA – 42mm.
Skin Biopsy Revealed: Epidermis was normal and dermis showing accumulation of basophilic mucoid material and collagen bundles. There was occasional macrophages and multinucleated giant cells compatible with pseudoxanthoma elasticum.
Colour Doppler study of kidney and renal arteries showed normal kidney size , shape, echo structure and punctate calcific areas on both renal cortex. Both renal arteries and interlobar arteries and aorta showed normal Doppler profile.
Doppler study of upper and lower limb arteries showed:-
Upper Limb: B/L subclavian , axillary, brachial , radial , ulnar arteries were anechoic with normal caliber and showing loss of normal triphasic blood flow with low resistance blood flow in them.
Lower limb: B/L femoral , popliteal and dorsalis pedis arteries were normal caliber with speaks of arterial calcifications seen in arterial wall at places and with loss of normal triphasic blood flow with low resistance.
Aorta and iliac arteries: Showed normal in caliber and size with normal spectrum of blood flow and no thrombus or stenosis. The patients was diagnosed to be a case of Pseudoxanthoma Elasticum with complications leading to peripheral vascular , renal and retinal involvement.
Treatment given: Capsule E, Tab Pentoxyphyllin and advised diet restriction , regular follow up.
DISCUSSION:
Pseudoxanthoma elasticum is a rare disease occurring in about 1 in every 160,000 population. Females are frequently affected. The basic defect lies in the elastic tissue. Typically it is first noticed during adolescence as yellow orange bumps on the side of neck. This entity has been observed in India and has been reported sporadically from all regions.
Aetiology:
Pseudoxanthoma elasticum is caused by genetic mutations that are inherited in either a dominant or recessive mode. A person with recessive form of the disease (most common) must posses two copies of the PXE gene to be affected, and therefore must have received one from each parent. In dominant form , one copy of the defective gene is sufficient to cause the disease. In some cases, a person with dominant form inherits abnormal gene from a parent with PXE, more commonly, the mutation , arise as a spontaneous change in the genetic material of the affected person. These cases are called “ Sporadic” and do not affect parents or sublings , although each child of a person with sporadic PXE has a 50% risk to inherit the condition.
Actual genetic defect is caused by different mutations or deletion in a single gene called ABCC-6 (also known as MRP6) located on chromosome 16. Although responsible gene has been identified, how it causes PXE is still unknown1.
It has been suggested that defects on glycosaminoglycans or proteoglycans might play a role in pathogenesis, bends of chondroitin sulphate, dermatan sulphate and hyaluronic acid are increased in the areas of calcification2.
An abnormality in cysteine proteinase of the fibroblasts has been demonstrated. It seems likely that an abnormal glycosaminoglycan secreted by fibroblasts is deposited on the surface of the elastic fibres and leads to fragmentation and calcification.
Pathology:
In skin lesions the elastic fibres in the mid dermis are clumped, degenerated, fragmented and swollen and abnormal fibres stains positively for calcium. The collagen fibres are also abnormal being split into small fibres. Similar changes occur in connective tissues of the media and intima of blood vessels, Bruch membrane of the eye and the endocardium and pericardium. Calcification has been reported in pulmonary and other visceras3.
Vascular involvement is generalized but may involve predominantly the larger arteries, the mesenteric , renal and visceral arteries or those of the extremities. Calcification of internal elastic lamina of the arteries leads to vascular obstruction.
CLINICAL FEATURES:
Skin changes: Lesion are small (1-3 mm in diameter), yellowish papule arranged on linear or reticular pattern and eventually forming plaques. Telangiectasia may be present. Areas involved are – fold of groin, arms, neck, axillary folds, armpits, perineum and mucous membrane. Skin is soft, lax, wrinkled and may hang in folds.
Eye: Angioid streaks represent defect or cracks in Bruch’s membrane. Angioid streaks are irregular jagged, curvilinear lines that radiate from the region of the optic nerve into the more peripheral retinal tissue. Other findings in PXE include salmon spots (areas of tissue atrophy) optic disc drusen (calcified deposits within the optic nerve head) and crystalline bodies (small yellow round subretinal lesions) and choroids neovascularization presented with visual loss (70%). If haemorrhage and choroiditis develops it may lead to blindness4.
Cardiovascular Changes:
• There may be intermittent claudication, diminished peripheral pulses, accelerated altheroma with hypertension5.
• Death commonly result from cerebral haemorrhage, coronary occlusion (angina/MI) or massive haemorrhage into the gut5.
• Cardiomyopathy and mitral value prolapse (5-8%) has been reported.
Associated abnormalities: May be associated with Osteitis deformans (Pagets disease) Osteoectasia, sickle cell disease, Marfan’s Syndrome and perforating elastosis.
Diagnosis:
Diagnostic criteria for Pseudoxanthoma elasticum (from Lewohl et al)6.
Major Criteria:
1. Flexural yellow cobblestone lesions.
2. Characteristic histopathological features of lesional skin using elastic tissue and calcium stains (e.g Van Gieson and Von Kossa).
3. Angioid streaks in the retina.
Minor Criteria:
1. Characteristic histological changes in non-lesional skin.
2. Family history of PXE in first degree relatives.
• It should be suspected in cases without skin lesions by obliterative arterial disease of early onset and unexplained gastrointestinal haemorrhage.
Management:
• The important aspect of treatment is to ensure that complications from blood vessels involvement are prevented or dealt with speedily by the appropriate specialist. Regular follow up with a specialist vascular surgeon and/or cardiologist is recommended.
• There is currently no effective treatment for skin lesions, but the appearance may be improved by plastic surgery.
• Restriction of dietary calcium has been tried with some benefits , but controversial.
• Laser photocoagulation, may be helpful in preventing further bleeding at the back of the eye.
• Genetic counseling may be helpful.
• Propranolol – to prevent development of aortic dilatation.
CONCLUSION:
Though incidence of haematuria is reported earlier in some cases, our case primarily presented with haematuria along with other usual complications. The probable mechanisms is due to microvascular involvement of kidney and urinary tract.
REFERENCE:
1. L Frank Glass/Shelli Marks, BS: Department of Internal Medicine and Pathology, Vuniversity of South Florida College of Medicine –Nov 2003 – 05.
2. Pasquali – Ronchette L, Pincellinc et al – Arch dermatol. Res 1986, 278, 386-92.
3. Goodmen RM, Simth E W, Paton D et al – “PXE”: Clinical and histopathological study medicine, 1963, 42, 297- 334.
4. Vitreous –Retina – Macula Consultant of New York – Angioid streaks and pseudoxanthoma elasticum.
5. Parker J C, Firedman –Kien AE, Levin et al . NEJM 1964/Kundrotus L, Novak J et al ; GI bleeding in PXE Am J Gastroenterol , 1988.
6. Lebwohl et al ; J Am Aacd Dermatol, 1994.
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CREUTZ FELDT-JAKOB DISEASE TRANSMITTED BY INTRAOCULAR LENS IMPLANT – A RARE CASE REPORT
Posted by on Thursday, 22nd July 2010
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.
CASE REPORT :
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.
ON EXAMINATION :
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.
DISCUSSION :
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.
REFERENCE :
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 IN A CASE OF FALCIPARUM MALARIA – A RARE PRESENTATION
Posted by on Thursday, 22nd July 2010
.
ABSTRACT
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.
KEY WORDS
Symmetric peripheral gangrene (SPG)
Falciparum malaria
Disseminated intravascular coagulation (DIC)
INTRODUCTION
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.
CASE REPORT
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
LFT :
Serum Bilirubin : Total 0.78mg%
Direct 0.26mg%
SGOT: 39U/L
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.
DISCUSSION
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.
CONCLUSION
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.
REFERENCE
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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RARE PUFFER FISH POISONING – A CASE REPORT
Posted by on Thursday, 22nd July 2010
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ABSTRACT:
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.
KEYWORDS:
Food poisoning, Ich thyotoxicosis, Tetrodotoxin, Puffer fish
INTRODUCTION:
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.
CASE REPORT:
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).
DISCUSSION:
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).
CONCLUSION:
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.
BIBLIOGRAPHY:
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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