News letter from Department of Medicine JSS Medical College Mysore JSS University MysoreNews letter from Department of Medicine JSS Medical College Mysore JSS University Mysore

CAPSULECAP ULESEditors: Dr. K.A.Sudharshanamurthy Dr. H.S.Devaraj Dr. SureshBabu.M Dr. Narahari,M.G

Dr. Sudharshana Murthy K.A.Professor & Head

Dept of Medicine

JSSMC & Hospital

Mysore

Editorial Splenic abscess in a case of Enteric feverDear Reader

t is indeed, a very pleasant task to present the next Iissue of CAPSULE. The facts

and issues are so numerous to share and discuss, but the platform and time constraints limit such a spirit only in documenting, reviewing and reflecting on interesting, unusual and rare cases in the Capsule. In order to overcome the limitations on interaction, the Department of Medicine, JSS Medical College and Hospital is organizing two day long State level CME programme JSS PG MEDICON 2010 focusing on the requirements of Post-graduate students of Medicine on 3rd and 4th September 2010. Eminent speakers, teachers all over from the state and also from outside are descending on to the venue to shower the pearls of their wisdom by discussing clinical cases and conducting interacting sessions on ECG, Radiology, ABGs and many other topics, which any Medicine post-graduate ought to master. We wish, this v e n t u r e w o u l d g e t a n overwhelming response from all the students and they would utilize the opportunity to enrich them with the latest knowledge delivered by the Masters.This issue of Capsule portrays three interesting and uncommon cases. We encourage your response and suggestions to improvise Capsule. Look forward to meet you at JSS PG MEDICON 2010.

With best regards.

SudharshanaMurthy,K.A.,Kiran,H.S, Narahari,M.G., Thippeswamy,VijayCheluvaraj, Tejaswini,Ashok,Nikhil Palrecha,Siddhivardhan,Venkatesh

Medicine 2ndUnit JSSMC &Hospital, MysoreAn 18 year old male presented with high grade fever with chills & rigors, joint pain,

upper abdominal pain, vomiting, cough with mucopurulent expectoration of 1 week duration. Patient was febrile, except for bilateral cervical lymphadenopathy, general physical examination was unremarkable. Optic fundus examination was normal. He had mild hepatomegaly and tender enlarged spleen of 4cm without any rub or bruit. Cardiovascular examination revealed systolic murmur at the left lower sternal border. The White Blood Count was 8300 cells/ mm3 with a neutrophilic predominance. ESR was 60mm/1hr and platelet count was 75000/mm3, without any suggestion of any hematological malignancy. Liver enzymes were elevated four fold without any other biochemical derangement. Widal test was positive and blood culture yielded Salmonella typhi growth. Tests for malaria, leptospira, dengue, ricketsia, mononucleosis and HIV were negative. Abdominal ultrasound revealed multiple hypoechoiec areas in spleen, largest one 5.2X3.7 cm volume around 40 cc suggestive of an evolving abscess with a differential diagnosis of infarction. Echocardiography revealed mild pericardial effusion with normal LV ejection fraction. There was no suggestion of any valvular abnormality or infective

endocarditis. Hemoglobinopthies and hemolytic anemias were ruled out by relevant tests because of their known associations with splenic abscess.

Despite on broad spectrum antibiotics patient continued to have fever. Based upon his blood c/s -Amikacin, crystalline penicillin was added and he responded well. A percutaneous drainage was not attempted as multiloculated or debris-filled abscess / multiple small abscesses was contraindication for drainage. A contrast enhanced CT scan revealed mild splenomegaly with multiple, irregular non-enhancing hypodense lesions in the splenic parenchyma with minimal left pleural effusion, normal appearing rest of the abdominal organs without any ascites or adenopathy : CT features are suggestive of a possible splenic abscesses/ infarction.

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!Discussion

Splenic abscess is an uncommon but potentially life-threatening disease with a reported frequency in autopsy series between 0.14% and 0.7%. About 600 cases have been described so far in the international literature. Recent advances in radiology have affected the diagnosis and management of

this disease entity. The clinical presentation is subtle and often diagnosis is delayed. Splenic abscess often occurs in the patients with recognized risk factors. These include the synchronous presence of conditions that compromise the immune system, such as endocarditis, diabetes mellitus, congenital or acquired immunodeficiency and the administration of immunosuppressive medication (e.g. post-transplantation or as part of the treatment of connective tissue disorders). Trauma is an additional predisposing factor for splenic abscesses. Common symptoms in patients with splenic abscess are fever, abdominal pain and nausea and vomiting. Ultrasound is used as a preliminary diagnostic modality, which is often followed by CT scan. However, ultrasonography can not discriminate between abscess and infarct in some cases, while computed tomography is the examination of choice. Splenic abscesses appear as focal areas of low attenuating well-defined lesion with rim enhancement; however, presence of gas is usually diagnostic. Ultrasound is almost sensitive as CT in demonstrating splenic abscess, but specificity is low. On US, abscesses appear as hypechoic or anechoic poorly defined lesions with irregular walls. If gas is present, high intensity with 'dirty' shadowing is apparent. Fungal abscesses on CT have a “wheel-within-a wheel” pattern due to a different intensity of vital fungal elements.

In contrast to previous reports (Streptococcus and Staphylococcus species predominant) a case series from Taiwan revealed GNB were the leading pathogens causing splenic abscess (55.2%). Among GNB, K. pneumoniae was the most frequently encountered pathogen (22.4%) and also came up with a novel finding that patients with GNB infection were prone to develop multiple splenic abscess (P = 0.036) and had a higher mortality rate. Splenic abscess may be solitary or multiple. Multiple abscesses are commonly encountered in immuno compromised patients. The predominant aerobic and facultative bacteria were E. coli, S. aureus, Streptococcus group D, K. pneumoniae and Proteus mirabilis. The predominant anaerobic bacteria isolated in a case series are: Peptostreptococcus spp. Bacteroides spp.Clostridium spp.Prevotella spp. A few cases with multiple splenic abscesses caused by S. typhi are described. Allal, et al.reported 400 patients with S. typhi and found splenic abscess in 8 (2%) cases; of these only one had multiple splenic abscess. The Taiwan series reports isolation of Salmonella species in 5 of 67 isolates; with a single case developing multiple abscesses, demonstrating its rarity.

Diagnostic fine needle aspiration of splenic abscesses is crucial to choose the most active antibiotics. Whereas blood culture isolates are generally monomicrobial, pus cultures from splenic abscesses are polymicrobial in almost half the cases. Therefore, clinical samples should be obtained from both blood and abscess. In immunocompromised patients, fine needle aspiration may also help in differentiating splenic abscesses from other splenic lesions that have the same appearance on imaging, such as lymphoma, metastasis, infarction, or hematoma. Moreover, splenic abscesses caused by disseminated fungal infections may be unrecognized in patients with AIDS who have life-threatening systemic illnesses.

Although antibiotics and splenectomy are traditionally considered the treatment of choice, in a few studies spleen-preserving management using percutaneous image guided drainage is favored; as splenectomy entails the risk of fulminant and potentially life-threatening infection. Percutaneous US- or CT guided drainage for single abscesses and splenectomy for multiple abscesses are reported as safe and effective treatment choices. The advantages of percutaneous drainage over surgical drainage are the low risk of intra-abdominal spreading, the absence of postoperative complications, including those due to anesthesia or wound infection, a shorter hospitalization time, lower costs, and better compliance of patients. As there are no standard rules set for aspiration of splenic abscess, operators have relied on their experience with liver abscess drainage and have demonstrated safety and success in at least a few cases: though not yet replacing the time honoured Splenectomy!

References: 1. Splenic abscess associated with

endocarditis.Robinson SL; Saxe JM; Lucas CE; Arbulu A; Ledgerwood AM; Lucas WF Surgery 1992 Oct; 112(4):781-6; discussion 786-7.

2. Management of splenic abscess: report on 16 cases from a single center. Giovanna Ferraioli, Enrico Brunetti, Rosario Gulizia, Giuseppe Mariani, Piero Marone, Carlo Filice International Journal of Infectious Diseases (2009) 13, 524530

3. Impending Rupture of Splenic Abscess in Enteric Fever. Vikas Jindal and V P Singh, Indian Pediatrics volume 45__october 17, 2008

4. Clinical characteristics and prognostic factors of splenic abscess: A review of 67 cases in a single medical center of Taiwan Kuo-Chin Chang, Seng-Kee Chuah, Chi-Sin Changchien,et.al, World J Gastroenterol 2006 January 21; 12(3): 460-464

5. Microbiology of liver and spleen abscesses I. BROOK and E. H. FRAZIER J. Med. Microbiol. - Vol. 47 (1998), 1075-1080 T) 1998 the Pathological Society of Great Britain.

6. Abscesses of the spleen: Report of three cases Constantin Fotiadis, Giagkos Lavranos, Pavlos Patapis, Gabriel Karatzas World J Gastroenterol 2008 May 21; 14(19): 3088-3091

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Subhash Chandra B.J., Malla Reddy, Narahari, M.G, Shashidar K.C., Aboobacker Siddiq. Medicine 5th unit JSSMC & Hospital Mysore.

A 35 year old male patient, agriculturist presented with chief complaints of generalized weakness, swelling over both the sides of the neck, axilla and groin, loss of weight since 1 month and fever of one week duration. Reformed smoker with occasional alcohol use, there was no significant family history.

General physical examination revealed pallor, cervical, axillary and inguinal lymphnode enlargement, which were tender, discrete and soft in consistency, not fixed to the underlying skin, with no sinus or scars and without local rise of temperature. Systemic examination was marked by presence of hepatosplenomegaly.

Investigations revealed Hemoglobin of 5.3g/dl, total leucocyte Count 2 lakhs/ mm3, Platelet count- 32000/mm3, ESR 110mm/hr. Peripheral smear showed reduced number of leucocytes with predominant myeloblasts (60%) and myelomonocytoid cells (30%). Platelets were severely decreased in number, Suggestive of Acute leukemia- Myeloid Myelomonocytic (M4). USG abdomen showed hepatosplenomegaly with multiple lymph nodes in pre and para aortic area, peri portal and

iliac groups. FNAC cervical lymph nodes showed numerous large cells with increase nucleo-cytoplasmic ratio, small mature lymphocytes and numerous multinucleated giant cells features suggestive of lymphoproliferative disorder. Patient got transferred to a oncology centre for further management two days after admission.

AML is the most common acute leukemia in adults and accounts for approximately 80 percent of cases in adults. In adults, the median age at diagnosis is approximately 65 years. The incidence increases with age with approximately 1.3 and 12.2 cases per 100,000 population for those under or over 65 years, respectively. The male: female ratio is approximately 5:3.

Patients with AML generally present with symptoms related to complications of pancytopenia (eg, anemia, neutropenia, and thrombocytopenia), including weakness and easy fatigability, infections of variable severity, and/or hemorrhagic findings such as gingival bleeding, ecchymoses, epistaxis, or menorrhagia. Palpable adenopathy is not common in patients with AML and significant lymph node enlargement is rare. Similarly, marked degrees of hepatomegaly and splenomegaly are uncommon and, if present, may suggest the possibility of acute lymphoblastic leukemia or evolution of AML from a prior myeloproliferative disorder (eg, blast crisis of chronic myeloid leukemia). These Extara Medullary Leukemia (EML) features are rare and controversy remains whether they confer a poor prognosis.

The disparous myeloblastic picture of peripheral smear and lymphoproliferative picture of FNAC report in the illustrated case opens up scope for considering differentials like Acute leukaemia of ambiguous/ mixed lineage warranting proteomics and other high end investigations. Categorizing the acute leukaemia takes priority in order to draw the line of management and prognostication.

Review of literature reveals description of widespread nodal involvement by acute myelocytic leukemia (AML), clinically mimicking non-Hodgkin's lymphoma, only twice. Prominent generalized lymph node involvement is very uncommon in AML at the onset. Only eight patients with bulky generalized lymphadenopathy at presentation, defined as adenopathy of more than 2 cm occurring in two or more major lymph node regions, have been described to date ; the prevalence of such an unusual presentation of AML among 293 consecutive patients done at that institution was very low (0.7%).

Though, 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia obviates the need for flowcytometry, Immunohistochemistry and other advanced tests in categorizing AML, the rare and unusual cases as one illustrated necessitate proteomics to design the line of management.

A number of prognostic factors related to patient and tumor characteristics have been described for AML. Of these, patient age at diagnosis, performance status, and karyotype have the most direct effect on treatment and should be a part of the initial evaluation of all patients with newly diagnosed AML. Gene mutation analysis, gene expression profiling, and microRNA profiling making an impact in prognostication and response to therapy are likely become part of the "routine" tests in characterization of AML in the near future.

Reference:1. The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. James W. Vardiman,Ju¨ergen Thiele,Daniel A. Arber,Richard D. Brunning,et al. Blood, 30 July 2009 volume 114, number 52. Acute myelocytic leukaemia manifested by prominent generalized lymphadenopathy: Report of two cases with immunological, ultra structural, and cytochemical studies Kathy Foucar, Department of Pathology, University of New Mexico, School of Medicine, Albuquerque, NM 87131 20063. Bulky lymphadenopathy in acute myeloid leukemia. Institute of Medical Semiology, Department of Hematology,Università Cattolica “Sacro Cuore”, Largo Agostino Gemelli, 8,I-00168 Rome, Italy 1998.

A Rare Case Of Acute Myeloid Leukemia With Generalized Lymphadenopathy

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Case Report

SudharshanaMurthy,K.A., Kiran.H.S., Vijay, Tejaswini, Ashok, Nikhil, Siddhivardhan, VenkateshMedicine 2nd Unit, JSSMedical College & Hospital.

A 50-year lady presented to the Emergency dept at around 1.00 pm with complaints of giddiness since morning, an episode of blackout lasting for 4-5 mins, and chest tightness/nausea/sweating following blackout. She did not give history of any co-morbid illnesses and she was not on any medications.The presenting ECG was as follows:The ECG had features of Antero-lateral Ischemia and QTc was grossly prolonged. As the patient had history of some neck surgery 3 months earlier (?Thyroid surgery), she was not thrombolysed.

Some Causes of QTc prolongation:1) Genetic causes:

p Congenital Long QT syndrome2) Due to pathological conditions:

p Electrolyte disturbances (like Hypocalcemia)p Ischemiap Hypothyroidism

3) Medicationsp Anti-arrythmic drugs (Amiodarone, Sotalol)p Tricyclic antidepressantsp Phenothiazedesp Some second generation antihistamines, like Astemizol

Investigation B.Urea- 56 mg/dL, S.Creatinine -1.9 mg/dL, Sodium- 138 mmol/L, Potassium- 3.7 mmol/L, Chloride- 101 mmol/L. Cardiac Enzymes: AST 92 U/L (normal 0-40), LDH- 1541 U/L (normal 230-460),CK-MB 41 U/L (normal 0-20) Troponin I- 0.093 ng/ml (0.04-0.49 ng/ml = Cardiac muscle injury; 0.50 ng/ml = Myocardial infarction) S.Calcium- 7.0 mg/dL (normal 8.8-10.8), S.Phosphorus- 7.3 mg/dL (normal 2.5-5.0) S.Magnesium- 1.9 mg/dL (normal 1.7-2.7)Total Proteins- 8.0 gm/dL, S.Albumin- 3.7 gm/dL), A/G ratio- 0.8At around 2:30 pm, patient had a generalised tonic-clonic convulsion, lasting for about 15-20 seconds. ECG repeated at that time was as follows:The ECG was suggestive of Polymorphic Ventricular Tachycardia (widened QRS complexes with varying morphologies). As the patient was vitally stable and conscious, the VT was treated medically and the ECG reverted as follows:With the above clinical & ECG features and as the patient had history of neck surgery 3 months earlier (?Total thyroidectomy), a probable diagnosis of Hypothyroidism and hypocalcemia (secondary to hypoparathyroidism following total thyroidectomy ) was made and she was initiated on IV Calcium Gluconate. The Thyroid and Parathyroid function tests confirmed the diagnosis: Thyroid profile: T3 0.94 (Normal 0.60-1.81 ng/ml)

T4 1.6 (Normal 4.5- 10.9 ìg/dl)TSH 90.28 (Normal 0.35-5.5 ìIU/ml)

S.Parathyroid hormone level: 4.0 (Normal 15.0-68.3 pg/ml)

Patient recovered with the above treatment at our hospital and was discharged subsequently with Thyroxine and oral calcium supplementation. ECG at the time of discharge was as follows:

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Varying morphology of QRS complexes with widening

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QTc approx 1.272 s : QT Prolongation

QT Interval

RR Interval

ST elevation with QT Prolongation

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Hypocalcemia:Hypocalcemia is the presence of low serum calcium levels in the blood, usually taken as less than 2.1 mmol/L or 9 mg/dl or an ionized calcium level of less than 1.1 mmol/L (4.5 mg/dL). Calcium regulation is maintained by parathyroid hormone (PTH), vitamin D, and calcitonin through complex feedback loops. These compounds act primarily at bone, renal, and GI sites. Calcium also is affected by magnesium and phosphorus. Causes:It manifests as a symptom of a parathyroid hormone [PTH] deficiency/malfunction, a Vitamin D deficiency, or unusually high or low magnesium levels.Few causes include: Eating disorders, Excessive dietary magnesium, prolonged use of medications/laxatives containing magnesium Absent parathyroid hormone (PTH): Hereditary hypoparathyroidism,Acquired hypoparathyroidism, Hypomagnesaemia, Following parathyroidectomy- "Hungry Bone Syndrome". following thyroiFectomy, the parathyroid glands are located very close to the thyroid and are easily injured or even accidentally removed during thyroidectomy. DiGeorge SyndromeIneffective PTH (Chronic renal failure, Absent active vitamin D, Decreased dietary intake, Decreased sun exposure, Defective Vitamin D metabolism, Anticonvulsant therapy, Vitamin-D dependent rickets, type I, Vitamin-D dependent rickets, type II) Pseudohypoparathyroidism, Deficient PTH ,Severe acute hyperphosphataemia Tumour lysis syndrome, Acute renal failureAs a complication of pancreatitisAs a result of hyperventilationAlkalosis, often caused by hyperventilationChelation TherapySymptoms: Petechia, Perioral tingling and paraesthesia, 'pins and needles' sensation over the extremities of hands and feet. This is the earliest symptom of hypocalcaemia. Tetany, carpopedal spasm are seen. Latent tetany can be unmasked by eliciting Trousseau sign and Chvostek's sign.Tendon reflexes are hyperactive.Hypotension may complicate acute hypocalcemia, particularly when rapidly induced either by EDTA or transfusion of citrated blood.In addition; decreased myocardial performance and even congestive heart failure (with or without hypotension) have been reported. Myocardial dysfunction is reversible with calcium repletion. Although the mechanism is undefined, calcium plays a critical role in excitation-contraction coupling and is required for epinephrine-induced glycogenolysis in the heart.Hypocalcemia characteristically causes prolongation of the QT interval in the electrocardiogram. Hypocalcemia prolongs phase 2 of the action potential with the impact modulated by the rate of change of serum calcium concentration and function of the myocyte calcium channels. Prolongation of the QT interval is associated with early after-repolarizations and triggered dysrhythmias. Torsades de pointes can potentially be triggered by hypocalcemia but is much less common than with hypokalemia or hypomagnesemia. Although electrocardiographic conduction abnormalities are common, serious hypocalcemia-induced dysrhythmias, such as heart block and ventricular dysrhythmias, are infrequent.ECG changes include: p Prolonged QTcp Prolonged ST intervalIrritability, confusion, hallucinations, dementia, extrapyramidal anifestations, and seizures are the neurological manifestations.

Management:p Two ampoules of intravenous calcium gluconate 10% is given slowly over a period of 10 minutes, or if the hypocalcaemia is severe, calcium chloride is given instead.p Maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)2-D3, i.e. calcitriol are often necessary to prevent further decline.p Correcting the underlying condition.

Reference:1. Risk factors for prolonged QTc among US adults: Third National Health and Nutrition Examination Survey. Benoit SR; Mendelsohn AB; Nourjah P; Staffa JA; Graham DJ Eur J Cardiovasc Prev Rehabil. 2005 Aug;12(4):363-8. 2. Hereditary long QT syndrome due to autoimmune hypoparathyroidism in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome. Meyer T; Ruppert V; Karatolios K; Maisch B J Electrocardiol. 2007 Nov-Dec;40(6):504-9.

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Book -

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To,

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With Best ComplimentsWith Best Compliments

MALE GAMETOCYTE TO FEMALE GAMETOCYTE (P.Vivax)“Darling !! We have had enough romance in this man's heart & blood.

We will soon unite in Mosquito and multiply and get children”.

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