FALCIPARUM MALARIA PRESENTING AS ACUTE PANCREATITIS
Posted by on Wednesday, 21st July 2010
ABSTRACT:
We report a case of Acute pancreatitis in a case of falciparum malaria. The incidence of other complications are common. The mechanism of this rare complication and its pathophysiology is reviewed. ( The Ind. Pract. 2005; 58(10): 649-651).
KEYWARDS:
Malaria (Plasmodium Falciparum Malaria), Complications, Acute Pancreatitis, Serum Amylase, Serum Lipase.
INTRODUCTION:
Malaria, a burning problem in tropical countries and a disease of global concern has a major preponderance in India affecting life of all ages and races. It complications are responsible for taking away a major fraction of patient death in our country. The acute and chronic complications are many. As far as falciparum malaria is concerned it has diverse life threatening complications. Acute pancreatitis is very rare but devastating complication of falciparum malaria which we have put as a case report.
CASE REPORT:
A 41 year old male presented in general medicine ward in October 2004 with history of fever of 5 days which was associated with chill and rigor. There was yellow coloration of urine and conjunctiva for 3 days and gradual decrease of urination for 2 days. There was 5-6 episodes of loose motions and vomiting and pain abdomen (confined to epigastic region) for 10 hours before admission. The patient was not an alcoholic. There was no previous such history of pain abdomen. There was no history of trauma to abdomen. He is not a known case of DM, HTN, SCD APD. There was no history of taking any drug.
On examination the patient was average built, conscious with moderate pallor moderate icterus with mild oedema (bilateral pedal) no lymphadenopathy with a pulse rare 92 per minutes, regular, BP 100/70 mm of HG, without any signs of dehydration. Abdominal examination revealed mild distension and diffuse tenderness maximum at epigastric area, smooth tender hepatomegaly ( 5 cm below the costal line) moderate non tender spenomegaly (3 cm below the left costal margin), mild ascites and diminished bowel sound. Cardiovascular system, respiratory system and other systemic examination revealed no abnormality.
INVESTIGATION
HB- 9.8gm%
TLC 10,200/mm2
DC N69%, E-1%, L30%, B0%, M0%
Widal test Negative
Microfilaria Negative
Serum Bilirubin Total 13.3mg%, Direct 10.4%
RBS 172mg%
SGOT 11IU/L
SGPT 138IU/L
Serum Alkaline Phosphatase 110 IU/L
S. Urea 106mg%
S.Creatinine 4.2mg%
Serum Amylase 2050 IU/L
Serum Lipase 3050IU/L
Serum Ca++ - 7.2gm%
HBs Ag Negative
HCV Ag Negative
Malaria Parasite Slide +ve
QBC pfr (++)
ICT pfr (+)
Ultrasonogram revealed hepatosplenomegaly and features of acute pancreatitis and mild ascites. CT scan of abdomen also revealed hepatosplenomegaly ascites and acute pancreatitis.
On the basis of blood report patient was treated along the line of complicated malaria with artesunate, injection cefipime, metronidazole injection, inject able pantoprazole, intravenous fluid and one unit of blood transfusion. The patient was conservatively managed for acute pancreatitis and nasogastric tube aspiration and nil orally for 5 days. The patient recovered within a span of 7 days after which the MP was negative. Serum amylase, serum lipase, Urea, Creatinine and bilirubin came down to 100IU/L, 230 IU/L, 28mg %, 0.8 mg%, 4.2 mg% respectively on 7th day. Repeat USG of abdomen revealed only mild hepatomegaly. The patients was relieved on 14th day of admission.
DISCUSSION:
Pancreatitis clinically presents with upper abdominal pain accompanied by elevated levels of pancreatic enzymes i.e amylase and lipase. The type such as acute chronic haemorrhagic, necrotic are distinguished by history, clinical , biochemical and radiological findings.
Acute pancreatitis presents as neusea, vomiting , anorexia, abdominal pain. Out of numerous causes of acute pancreatitis malaria is rare. But it must be looked for in tropical country like India with high prevalence of malaria.
Falciparum malaria is the deadest among all other types of malaria with varied complications, multiorgan involvement and diverse sequlae. The parasite may affect pancrease causing acute pancreatitis or acute haemorrhagic pancreatitis. The clinical and laboratory findings follow similar pattern of other causes of acute pancreatitis.
The pathogenesis may be initiated by sequestration of parasite in the organ, blood vessels or ducts, damaging acinar cells by premature activation of digestive enzymes with cells. The damaged acinar cells initiate inflammation, activation of platelets and compliment system, which leads to release to cytokines (e.g TNF - , IL 1, NO, PAF), free radicals and other vasoactive substances. These further directly damage the gland and may cause pancreatic oedema, necrosis, ischaemia and capillary leak syndrome. Tehse lead to a vicious inflammatory cycle damaging further pancreatic tissue. Association of sepsis further leads to organ damage and complications.
Malaria presenting with classical symptoms and signs of acute pancratitis along with other organ involvement may be difficult to correlate. The abdominal pain may be sharp, sudden or constant may be localized to epigastric,periumbilical, block or lower chest. But common presentation in malaria is fever, icterus with distended abdomen, diffuse or localized tenderness. Grey Turners signs or Cullen sign may be noted in advanced cases.
Blood count and chemistry panel usually distinguishes pancreatitis from other acute abdominal causes, Test of malaria (MP, Slide , QBC, ICT) determines malaria aetiology, Increased TLC, Hyperglycaemia, decreased Ca++, Increased alkaline phsophatase, S. Amylase, S. Lipase reflects pancreatic damage.
Serum amylase has low sensitivity (75-92%)and Specificity (20-60%) but is used to confirm acute pancreatitis , when upper limit is raised 3-6 times of normal specificity increases. Serum amylase level is raised 2-12 hours after pancreatic insult and peaks 12-71 hours after.
Serum lipase having sensitivity 86-100% and specificity of 50-99%. Serum lipase raised 4-8 hours after signs and symptoms and peaks at 24 hour and decrease over 8-14 days.
Other recent markers are immunoreactive cationic trypsin, pancreatic elastase 1 and phospholipase.
Although USG and Ct scan of abdomen makes the diagnosis easy, cholangio-pancreatography may be accompolished bu ERCP or MRCP.
The primary treatment of acute pancreatitis with malaria is to treat the cause i.,e malaria. The treatment of acute pancreatitis is primarily supportive providing adequate hydration, pain relief and pancreatic rest by nasogastric suction and nil orally. Antibiotics are added to prevent sepsis or necrotic pancreatitis with setting of multiorgan involvement.
The prognosis of acute pancreatitis with malaria depends on the stage of presentation, haemorrhagic pancreatitis bears poor prognosis.
CONCLUSION
Falciparum malaria which has various complications may present as an acute pancreatitis, along with other organ affection. This is a rare condition and must be in mind of clinicians when patient presenting with clinical features of malaria, with pain abdomen , vomiting and localized abdominal tenderness.
A high index of suspicion and thorough clinical examination and investigation are the ways to diagnose the complication i.e, acute pancreatitis. Specific antimalarial drugs are the primary modalities of treatment, along with the conservative management for acute pancreatitis.
REFERENCE:
1. Von Sonnenberg F, Los Cher T, Nothdurgt HD, Prufer L @ Pubmed . PMID : 3519146.
2. Michelle M, Piet Zak MD (1) Dan W Thomas MD (2).
3. Parenti DM, Steingberg W, Kang P Infectious causes of ac pancreatitis , 1996; 13(4) 356-71.
Rate It
ATYPICAL PRESENTATION OF HERPES SIMPLEX ENCEPHALITIS
Posted by on Wednesday, 21st July 2010
ABSTRACT:
Herpes simplex virus (HSV) encephalitis usually caused by HSV1 is gravest and commonest form of acute encephalitis. It is usually present with fever, headache, seizure, confusion, stupor and coma. Psychosis may be associated with these manifestations. Here we are reporting a case of clinico-radiologically diagnosed case of HSV encephalitis that present predominantly with psychosis and make diagnostic dilemma. (The Ind. Pract 2005; 58 (1):38-39.
KEY WORDS:
Herpes Simplex Virus, Encephalitis, Psychosis
INTRODUCTION:
Among all acute encephalitis 10% of cases are due to HSV. It is usually present like other acute encephalitis. Psychosis is a distinct feature due to involvement of temporal lobe, medial and orbital part of frontal lobe. CT scan imaging may identify the cerebral lesion at temporal and frontal lobe. Fatality rate varies between 30-70%. Early presumptic diagnosis with the help of clinical examination, C.S.F. examination and radio imaging and early therapeutic intervention with acyclovir may save the life of the patient. C.S.F. PCR is the diagnostic approach now for herpes simplex encephalitis.
CASE REPORT:
A 38 year old male presented with psychotic behavior or last 20 days. He was febrile for about 6 days 2 weeks back. Fever was typically low grade, contunuosu. With the onset of fever he starts incoherent talk.
He was also unable to recognize the known persons. His speech frequency was very much decreased and he was reluctant to take food. He was admitted to local private hospital on days of his illness where his CS examination was done. At that time his CSF cell count was 296/cumm, mostly lymphocytes, protein 72mg% and sugar 48mg%. His treatment was started there in the line of TB meningitis but patient gradually deteriorated. Due to his uncontrolled psychotic behavior, psychatric consultation was done, treated with haloperidol. But patients psychosis did not improve. Rather his bladder and bowel control was lost.
On the day of our hospital admission patient was febrile, drowsy, disoriented, illusion and auditory hallucination were present. Sensory aphasia, inhoherent talks were associated with those features. His plantar reflex was B/L extensor and gait unsteady. Investigation revealed WBC 11100/cumm. ESR 15mm and RBS 127mg% DC N 51% and L 49%. Repeat C.S.F. examination was done which revealed total WBC count 76/cumm mostly lymphocytes, protein 28 mg% and sugar 78 mg%. CSF contained plenty of RBC. CT scan of brain showed hypodense area at B/L temporal and fronto medial lobe (Fig. 1 and Fig 2) suggestive of HS encephalitis. Treatment was started with acyclovir 500 mg IV 8 hourly with monitoring pf S. Creatinine level. On 10th day of therapy patients psychosis decreased, was able to recognize his wife and son and plantar become flexor, though auditory and gustatory hallucination still persisted.
DISCUSSION:
HSV 1 and 2 infection can manifest a spectrum of illness from stomatitis and progenitor lesion to facial nerve palsy and encephalitis. Encephalitis is due to HSV1. The unique localization of the disease in the temporal lobe may be explained by the virus route of entry into the CNS1. The lesion takes the form of haemorrhagic necrosis of temporal and medial part of frontal lobe2. Lesion of these areas in imaging study with CT or MRI is highly suggestive3. Patients with Japanese encephalitis display abnormalities of thalamus, basal ganglia and midbrain. Other forms of viral encephalitis imaging studies are non- specific.
Manifestations like hallucination, anosmia, personality changes, bizarre behavior or delirium, aphasia usually observed in H.S. encephalitis. Temporal lobe seizure usually seen in ECG. Affection of memory can be recognized in the convalescent state.
CSF often cloudy due to RBC as well as WBC protein may be raised but sugar usually normal. In minority of cases, low sugar in CSF may confuse with TB or fungal meningitis. Test for detection of HSV in the CSF by PCR are useful in diagnosis while virus is replicating in first few days of illness.
Our patient presented at OPD after 3 weeks of illness when the absolute ways to establish the diagnosis is fluorescent antibody study and viral culture of brain tissue obtained by biopsy. Avoiding this hazardous procedure, we treated the patient with empirical antiviral agents based on compatible clinical, radiological and CSF findings. Treatment option for HSE is acyclovir in the dose of 30 mg /kg/day for 10-14 days5. Our patient was responding well with above mentioned treatment. After one month follow up , patient improved with mild psychotic behaviour, gaustatory hallucination and depression.
REFERENCES:
1. Davis L.E., Joshson R.T.: An explanation for localization of herpes simplex encephalitis. Ann Neural 1979; 5: 2.
2. Adams H. Miller D: Herpes Simplex encephalitis: A clinical and pathological analysis of twenty two cases. Post Grad M.D. J 1973; 49:93.
3. Davis J.M. et al : CT of herpes simplex encephalitis with clinico pathological correlation. Radiology 1978; 129:409 17.
4. Lakeman F.D., Whitley R.J. et al : Diagnosis of Herpes simplex encephalitis: Application of PCR to CSF from brain biopsied patient correlation with disease. J. infect disease 1995; 171: 857.
Rate It
NEWER THERAPEUTIC OPTIONS IN SICKLE CELL DISEASE
Posted by on Wednesday, 21st July 2010
INTRODUCTION
Sickle cell disease is an autosomal dominant disorder, sickle haemiglobin is the abnormal haemoglobin  chain glutamin acid is replaced by valine. Sickle haemoglobin has the unique property of forming polymersdeoxygenated state. These polymers deform the RBCS to sickle cell. Formation of polymers depends on the concentration of HbS inside the cell. So small reductions in HbS concentration inside the cell might result in significant clinical benefits. That is the reason why sickle cell trait is clinically silent were the HbS concentration is low. With better understanding of pathophysiology of sickle cell disease and its complications, it treatment has also progressed.
Among the haemolytic anaemias, vasoocclusive features are unique in SCD. Now it is well understood that vasoocclusion and tissue ischaemia in SCD involve not only the polymerization of HbS but also interaction between RBCs, endothelium, leucocytes, platelets and plasma factors. Intracellular polymerization of HbS is decreased by a rise in foetal haemoglobin and there increasing HbF is the most clinically studied approach against sickling. Infections, brain injury, renal disease , pain priapism can now be prevented. Complications from lung injury, surgery and transfusion can be minimized.
Management of SCD
Apart from general measures and treatment for symptomatic relief , now the newer therapeutic agents are directed towards prevent of complications.
THERAPEUTIC STRATEGIES FOR PREVENTION OF COMPLICATIONS
Sickling can be interrupted at several key pathways:
1. HbF Augmentation
Most promising agent in hydroxyurea, a ribonucleotide reductase inhibitor, causes myelosuppressive induced HbF synthesis, resulting in improved red cell survival and decreased sickling. Hydroxyurea is orally active, effective , safe in short term and beneficial in most patients, in the dose of 10-15mg/kg to a maximum of 35 mg/kg. Before starting hydroxyurea, base line evaluation like blood counts, MCV, HbF concentration and serum chemical values and test for pregnancy ( a contraindication) to be done. Blood counts should be performed every 4-6 weeks intervals, granulocyte count should be at least 2000/mm3 and platelet counts at least 80,000/mm3 before or during treatment. An initial Hb concentration below 5.5 gm% is not a contraindication to treatment with hydroxyurea. Adults with higher TLC and reticulocyte counts and larger treatment associated decreases in these counts tends to have greater increases in HbF production and hence better response to hydroxyurea. Although hydroxyurea lowers pain episodes, pulmonary events and hospitalizations, 40% of treated patients do not respond or have progressive organ failure, the reason for this is yet to be settled.
Clinical advances in treatment of SCD
Clinical Features Interventions
1. Pain Prevention with hydroxyurea
Patients controlled analgesic devices
Newer NSAIDS
2. Infection vaccine Prophylactic penicillin and pneumococcal
3. Anaemia Phenotypically matched RBCs
4. Lung injury prevention Hydroxyurea
Antibiotics (Macrolides)
Transfusions
Screening for pulmonary hypertension
5. Brain Injury prevention Screening with transcranial Doppler , MRI, neurocognitive testing
6. Renal ACE inhibitors for preteinuria
Improved renal transplantation
7. Call bladder disease Laparoscopic cholecystectomy
8. Surgery / anaesthesia safety Preoperative transfusion
9. Priapism Adrenergic agonist
Antiandrogen therapy
10. Avascular necrosis of hip Decompression coring procedures
11. Severe disease (recurrent acute chest syndrome, pain crises or CNS disease) Allogenic BMT (< 16 years)
Chronic transfusion and /or hydroxyurea
12. Neonatal screening
13. Family counseling
Other drugs which can increase HBF concentration are short chain fatty acids like valproic acid, 2-deoxy- 5 azacytidine , erythropoitein.
Other emerging therapeutic agents
Drug Mechanism Benefits
1. Clotrimazole Inhibits red cell Gardos channel Red-cell rehydration
2. Sulphasalazine Endothelial Activation Antiadhesion therapy
3. Deferiprone Chelete membrane iron Antiadhesion therapy
4. Acenocumarol, heparin Decrease thrombin Antiadhesion therapy
5. Pheresis Decrease HbS Transfusion therapy
6. Allogenic Haematopoietic stem cell transplantation
7. Genetherapy
a. Direct gene replacement Direct delivery of - globin gene.
b. Indirect gene therapy Srythropoitin delivery
2. Antisickling agent (through multiple pathway)
Nitric oxide (NO) is a critical factor in the pathphysiology of SCD and hence a potential treatment option. NO regulates vessel tone , endothelial adhesion, leucocytes and platelet activity, an important factor in ischaemia reperfusion injury and sickle cell induced ischaemia. In SCD, more adhesion molecules are produced due to decreased availability of NO. Oral arginine supplementation induces NO production, reduces red cell sickling by inhibiting the Gardos channel (Calcium activiated K = Channel). Treatment of sickle cell patients with NO or its precursor L arginine have shown promising antisickling activity with vasodilator properties. NO or arginine supplementation may be synergistic with hydroxyurea and seems to further increase. No release and decrease adhesive molecules.
CONCLUSION:
The need to study new applications of current treatment and to devise new treatments direct at disrupting multiple factors of the pathophysiology of the disease remains most important. New therapeutic options like hydroxyurea. No or L-Arginine, BMT, gene therapy appears promising. While awaiting the new treatments for the underlying disease, several partial problems remains unsolved. For example, how should the acute chest syndrome be managed, which patients should undergo exchange transfusion? How aggressively should be blood pressure be lower to decrease the risk of stroke? Can we better understand the cause of striking variability in sickle cell disease, so that hazardous treatment can be directed to the patients who are most likely to have the worst disease complications?
REFERENCES:
1. Bunn H.F. Pathogenesis and treatment of sickle cell disease. N. Engl J Med 1997; 337:762-9.
2. Steinberg M.H. Management of sickle cell disease. N. Engl j Med 1999;340:1021 30.
3. Morris C.R., Kuypers A., Larkin S et al : Arginine therapy : a novel strategy to induce nitric oxide production in sickle cell disease. Br J Haematol 2000; 111-498-500.
4. Vichinsky E . New therapies in sickle cell disease. Lancet 2002; 360: 629-31.
Rate It
UNCOMMON PRESENTATON OF HYPOGONADISM AND HYPERTENSION IN A CASE OF SICKLE CELL DISEASE- A CASE REPORT
Posted by on Wednesday, 21st July 2010
ABSTRACT:
Sickle cell haemoglobinopathy, a common haemolytic disease predominant in Western part of Orissa is a multisytemic disease, with varied manifestation. Through some case of nephropathy has been reported, earlier here we report a case of sickle cell disease (SED who had primary hypogonadism, hypertension and sickle cell Nephropathy. The pathogenesis and management are reviewed,.
KEY WORDS.
Sickle cell disease, primary hypogonadism, hypertension and sickle cell Nephropathy.
INTRODUCTION
Sickle cell haemoglobinopathy occurs due to genetic defect where due to mutation of  globin the 6th amino acid is changed from Glutamic acid to Valine. Due to dexoygenation there occurs structural changes in RBC Clinically the disorder manifests as chronic haemolysis repeated infection growth retardation and sickle cell crisis. The crisis includes alpastic crisis haemolytic crisis sequestration crisis and vasoocculsive crisis. Renal complications are encountered in some cases where the patient presents with haematuria proteinuria, renal insufficiency.
CASE REPORT
A 21 years male was admitted to this hospital in July 2005 with history of fever and jaundice for 5 days generalized pruritus for 4 days and decreased uriniation for 4 days. He had gradual diminished of vision of right eye since 5 years. He had taken Blod transfusion 2 months back at local hospital. On enquiry it was found that another brother who had sickle cell disease died 3 years back, due to vasoocculsive crisis. Both parents were found to be sickle cell trait. The patient had normal milestones of development but there was retarded development of secondary sexual characters and gyaecomastia since last 4 years (Fig.1.2)
On examination the patient had severe pallor and icterus, Blood pressure was 160/90 mmHg in both upper limbs. Pulse rate 110/min regular Temperature 100.20F respiration rate 18/minute. Per abdominal examination revealed moderate hepatomegaly and moderate spelenomegaly. He had bilateral gynaecomastia with sparse public and axillay hairs and facial hair. Both the testis volume were reduced (2.5 to 3 cm) soft with normal testicular sensations. Other systemic examinations including higher intellectual function were normal.
The laboratory examination showed:-
Hb:- 6.6% TLC- 8400/mm3, D/C N 68 E 2L 30 M0 B 0
Serum Billrubin Total 21 mg/dl
Direct 19 mg/dl.
S.G. O.T - 58IU/L
S.G. P.T - 57 IU/L
S. Alk Phospatase- 338IU/L
Hb electrophosis showed SS band.
Urine analysis showed Albumin (++) with granular cast and RB Ci 30- 40/HPF and 24 hour urine protein was 300mg/in 24 hour with urine output- 2 Litres.
Serum Zn- 7.5 (11.5-18..5 ml/L)
Untrasonogram of abdomen showed moderate hepatomegaly, spelnomegaly (18cm) with coarse echotexture with spotty calcification. Both kidneys were normal size(11.0cm x 4.5cm) with diminished corticomeduallry differentiation.
Chest x-ray and skull X- ray were normal.
Foundscopy revealed papilloedema (Rt eye) with Grade II hypertensive retinopathy. Visual acuity was 6/60 in right eye and 6/9 in Left eye.
Fasting lipid profile showed TC-109mg%, HDL-25mg% , LDL-50mg% , TG-376mg%, VLDL-75.30mg% , 212.86ngm/dL (270-1070mg/dl)
Hormonal assay showed Testosterone FSH 8.41 IU/ml, LH17.97IU/Ml, Prolactin 5.45ngm/ml, TSH-3.79IU/ML, (0.5-4.7U/ml) 2.72U/ml) (1.6-23.0 ngm/ml).
Kidney biopsy showed features of focal segmental glomerulosclerosis (Fig-3, Fig-4)
Patients was treated with antimalarial (Artesunate) antibiotic (Taxim) Pentoxyphylline, folic acid arginine Antihypertensive- Imandipril-10mg (ACE inhibitor) was started and responded well with normalization of BP. After 15 days of treatment the BP was controlled at 120/80 mm Hg, with reduction of Proteinuria. His serum bilirubin came down to 4.6mg/dl (total) and 3.8mg/dl (direct). The patient was discharged.
On subsequent follow up (after 45 days of discharge) 24 hours urine protein 25mg/24 hours, Urine output 2.5 Litres, BP was 120/70.
DISCUSSION:
The gonadal dysfunction as noted in sickle cell disease most often is attributed to primary gonadal failure. Levels of LH are usually increased in sickle cell disease. changes in FSH are usually inconsistent . Testosterone levels are almost always low in male adolescents and adults with sickle cell disease & these levels may respond poorly to GnRH stimulation.
Extreme delay in secondary sexual character is usually confined to males. Testicular size and volume are reduced and testicular histology showed immaturity of seminiferus tubules and replacement by hyaline materials secondary sexual character such as bearded growth, public and axilary hair are retarded.
The determinant of this type of growth may be chronic anemia patients with higher fetal hemoglobin have normal epiphyseal closures. Zinc level are lower in patient with sickle cell disease and studies have shown that zinc supplementation increased growth of body hair, increased testosterone levels and improved testosterone response to LHRH.
Sickle cell nephropathy in the form of glomerular disease occurs in 15 to 30% of sickle cell disease. Usually 15-30% patients develop proteinuria in the first 3 decades. The pathology is usually focal segmental glomerulosclerosis chronic renal failure can be predicted by presence of worsening anaemia, proteinuria, nephritic syndrome and hypertension. ACE inhibitors and ARB retard the progression of renal disease by lowering systemic & glomeruocapillary hypertension.
Hypoxia of renal medulla may also cause papillary necrosis. Coinheritance of microdeletion in  gene appear to protect against development of nephropathy. Cortical infarcts can cause persistent haematuria, pipiallry infects occurs in 50% of patients with sickle cell trait. Painless gross haematuria occurs with higher frequency in sickle cell trait than sickle cell disease.
Ultrasound examination may reversal a focal or diffuse increased echogenecity which is predominant in sickle cell disease. In the medulla renal tubules and vasarecta involvement can occur. Tubular changes results in atrophy dilatation, proteinacous cast and the so called thyroidization of renal medulla also occur.
In sickle cell disease the GFR is markedly elevated in young patients but decreases with age. As age increases the effective renal blood flow. effective plasma renal flow are decreased. Increased GFR, ERRF in sickle cell disease is usually due to increased synthesis of prostaglandins in early part which decrease in later life.
CONCLUSION
Sickle cell disease is a fairly common disease in this belt of India but usually the focus is directed towards managing vasoocclusive crisis.
But proteinuria, hypertension are the harbinger of sickle cell nephropathy and will respond to ACE inhibitors and ARB. The hypogonadism may be treated in early life by good nutrition, prevention of anaemia and zinc supplementation.
Rate It
ASSOCIATION OF PLEURAL EFFUSION (LEFT) WITH PANCREATIC PSEUDOCYST
Posted by on Wednesday, 21st July 2010
ABSTRACT:
We report a relatively uncommon association of massive pleural effusion (left) with pancreatic pseudocyst in an adult male patient. The pathophysiology, clinical features diagnosis and management of this conditions are reviewed. (The Ind. Pract 2004; 57(8): 553-554).
Key Words: Pancreatic Pseudocyst, Pleural Effusion
INTRODUCTION
Pseudocysta are localized collections of panecreatic secretions that lack and epithelial lining and persist for more than 4 weeks. In the past pseudocysts were detected. indirectly by clinical suspicion, appearance of a palpable abdominal mass and from barium contrast studies that demonstrated a mass. The advent of pancreatic imaging by ultrasonography and CT Scan has lead to the realization that pseudocysts appear in 10% patients with acute pancreatitis.
A variety of clinical and radiographic finding have been associated wit pancreatitis and pleural effusion is one of them. pleural effusion may be bilateral, confined to left side or rarely right sided and may be massive.
CASE REPORT
A 50 year old male patient admitted with history of chest pain for 1 month, swelling of abdmen with upper abdominal pain for 1 month, loss of appetite with nausea for 15 days and dyspnoea for last 3 days. Six months prior to admission he was provisionally diagnosed to be a case of pulomonary tuberculosis with left sided pleural effusion and was on treatment with ATT (4 drugs) for 6 months without any clinical improvement. He is not a known case of DM, HTN, SCD. No history of intake of other drugs. He is a chronic alcoholic for last 20 years.
On examination the patients was of average built with mild pallor, no icterus, no lymphadenopathy, with a pulse rate of 76 per minute, regular BP=118/80 mmHg. Cardiavascular system examination revealed apex beat Rt. 5th ICS. Chest examination revealed trachea shifted to right side. on left side reduced movement , stony dull percussion note, vocal response absent, breath sound diminished. Per abdomen examination revealed mild hepatomegaly with a firm intra abdominal swelling palpable in the middle left upper abdominal region, non tender with irregular margin.
INVESTIGATIONS
Hb = 8.6gm%
TLC = 8000/mm3
DC =N-60% , E-4%, L-36%
ESR =25mm 1st hr
FBS = 92mg%
Urine =NAD
S. urea = 38mg%
S. Creatinine = 1.1 mg%
Na+ = 135m.mol/L
K+ = 3.4 m.mol/L
Pleural fluid analysis revealed , coffee coloured, haemorrhage fluid with TLC could 700 mm3 mostly mestothelial cells mixed with cellular elements of blood. No malignant cells seen. Biochemical study revealed glucose- 60mg% protein 1.6mg%. LDH- 2280IU/L Amylase- 30 IU/L.
Chest X- ray (PA view0 reveals massive pleural effusion (lt) with trachea shifted to rt.side. USG abdomen and pelvis reveals head of pancreas normally seen but the body and tail could not be visualized. A large cystic lesion of 15cm x 12cm with echogenicity seen with left sided pleural effusion.
The patient was diagnosed as a case of pancreatic pseudocyst with left sided pleural effusion due to acute pancreatitis probably alcohol induced. Pleural tapping was done and about 3000ml of haemorrhagic fluid was drawn out. He was put on of loxacin. valdecoxib, haematinics and other supportive treatment. The patient showed marked improvement during hospital stay and planned for surgical management for the existing pseudocyst.
DISCUSSION
Pancreatic pseudysts are collections of tissues, fluid debris enzymes and blood which develop over a period of 4 weeks after the onset of acute pancreatitis and constitute about 10% of patients of acute pancreatitis. It is encountered most frequently with alcoholic panaceatitis. Pseudocysts associated with pleural effusion are most common on the left but may be bilateral and rarely limited to right pleural space (Gumaste Singh, Dave et a, 1992) it is assumed to be a new prognotic parameters for acute pancreatitis (Lankisch Droge, Becher et al1994).
Psyeuodycysts lack epithelial lining and disruption of the pancreatic ductal system is common. Approximatelty 85% are located in the body or tail of pancreas and 15% in the head. If the pancreatic duct disruption is posterior, an internal fistula may be develop between the pancreatic duct and the pleural space producing a pleural effusion which is usually left sided and often massive. Conservative therapy is indicated if the pseudocyst is shrinking evidenced by serial ultrasound and minimal symptoms pseudocysts (every 3 to 6 months) Long acting somatostatin anagogic octreotide which inhibits pancreatic secretion is useful in cases of pancreatic ascetics with pleural effusion.
Pseudocyst with communicating duct if strictured require internal surgical or endoscopic drainage. Transgastric percutaneous approach is favoured. Associated massive left sided pleural effusion often required thoracentesis or chest tube drainage. A disrupted pancreatic duct can be treated by stenting.
CONCLUSION
Association of the left sided massive pleural effusion with pancreatic pseudocyst is relatively uncommon. However, additional studies are needed to substantiate these results.
REFERENCES
1. Gumaste V., Singh, V., Dave P. Significance of pleural effusion in patients with acute pancreatitis. Am J. Gastroenterilogy 1992; 87: 871.
2. Lankisch P.,G. Droge M and Becher R. Pleural effusion : A new negative prognostic parameter for acute pancreatitis. Am J Gateroesterol 1994; 89: 1849.
3. Slesinger and Fordtrans Gastrointestinal and liver disease (6th edn) vol1 Sleisenger Feldman Scharshmidt Klein (W.B Saunders Co) 815:826:836.
4. TB of Gastroenterology (Vol-II) 2nd Edn Year 1995 (T. Yamada. J.B. Lippincott Co. Philadelphia ) page 2078-84.
5. Harrisons principles of Int. Medicine 15th Edn Vol 2 year 2001: Page-1798.
Rate It
Why we are No. 1 › 
Category (
Views ( 8537 ) | User Rating
