DAY OF FEVER

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CLINICAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH FEBRILE THROMBOCYTOPENIA IN TIRUNELVELI MEDICAL

COLLEGE

DISSERTATION SUBMITTED TO THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY, CHENNAI In partial fulfilment of the requirements for the degree of

M.D. BRANCH – I (GENERAL MEDICINE) Registration Number: 201711366

DEPARTMENT OF GENERAL MEDICINE TIRUNELVELI MEDICAL COLLEGE HOSPITAL

TIRUNELVELI – 627011 MAY-2020

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BONAFIDE CERTIFICATE

This is to certify that the dissertation entitled “CLINICAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH FEBRILE THROMBOCYTOPENIA IN TIRUNELVELI MEDICAL COLLEGE” submitted by Dr. S.SARAVANAN, to the Tamilnadu Dr.

M.G.R Medical University, Chennai, in partial fulfillment of the requirement for the award of M.D. Degree Branch – I (General Medicine) is a bonafide research work carried out by her under direct supervision & guidance.

Professor & Head of the Department, Department of General Medicine

Tirunelveli Medical College, Tirunelveli.

Unit Chief,

Department of General Medicine Tirunelveli Medical College,

Tirunelveli.

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CERTIFICATE BY THE DEAN

I hereby certify that this dissertation entitled “CLINICAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH FEBRILE THROMBOCYTOPENIA IN TIRUNELVELI MEDICAL COLLEGE” is a record of work done by Dr. S.SARAVANAN, in the Department of General Medicine, Tirunelveli Medical College, Tirunelveli, during his postgraduate degree course period from 2017- 2020. This work has not formed the basis for previous award of any degree.

Date :

Place : TIRUNELVELI The DEAN

Tirunelveli Medical College, Tirunelveli - 627011.

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DECLARATION

I solemnly declare that the dissertation entitled “CLINICAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH FEBRILE THROMBOCYTOPENIA IN TIRUNELVELI MEDICAL COLLEGE” is done by me at Tirunelveli Medical College Hospital, Tirunelveli Under the guidance and supervision of Prof.Dr.G.Rathnakumar M.D, the dissertation is submitted to The Tamilnadu Dr. M.G.R. Medical University towards the partial fulfilment of requirements for the award of M.D. Degree (Branch I) in General Medicine.

Place: Tirunelveli

Date: Dr S.SARAVANAN,

Registration Number: 201711366 Postgraduate Student,

M.D General Medicine, Department of General Medicine,

Tirunelveli Medical College Tirunelveli.

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CERTIFICATE – II

This is to certify that this dissertation work entitled “CLINICAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH FEBRILE THROMBOCYTOPENIA IN TIRUNELVELI MEDICAL COLLEGE” of the candidate Dr.S.SARAVANANwith registration Number 201711366 for the award of M.D. Degree in the branch of GENERAL MEDICINE (I). I personally verified the urkund.com website for the purpose of plagiarism check.

I found that the uploaded thesis file contains from introduction to conclusion page and result shows6 percentageof plagiarism in the dissertation.

Guide & Supervisor sign with Seal.

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ACKNOWLEDGEMENT

I wish to express my heartfelt gratitude to our Dean Prof.Dr. S. M. .Kannan M.S., MCh., Tirunelveli Medical College for allowing me to do the study in this institution.

I would like to express my humble thanks to our professor & Head of the Department Prof .Dr .M.Ravichandran M.D., Department of General Medicine.

I express my sincere thanks to my renowned teacher and my guide Dr.G.Rathnakumar M.D., Professor, Department of General Medicine, Tirunelveli Medical College for his guidance, valuable suggestions and constant encouragement throughout the study.

I express my sincere thanks to my former professors, Dr.S.Arumugapandian @ Mohan, M.D., Dr.S.S.Nazar M.D., for their constant support, encouragement and suggestions which helped me greatly to expedite this dissertation .

I am greatly obliged to Dr.S.Jawahar M.D, Dr.Govindarajan M.D, Dr.Rajkumar M.D, Assistant Professors, Dept .of General Medicine for their valuable suggestions in preparing this dissertation.

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CONTENT

S.NO TITLE PAGE.NO

1. INTRODUCTION 1

2. REVIEW OF LITERATURE 3

3. STUDY JUSTIFICATION 31

4. AIM OF THE STUDY 32

5. MATERIALS AND METHODS 34

6. STATISTICAL ANALYSIS 37

7. RESULTS 38

8. DISCUSSION 80

9. CONCLUSION 85

10. LIMITATIONS OF 86

11. BIBILIOGRAPHY 12. MASTER CHART

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1.INTRODUCTION

Low number of platelets will be in the blood circulation in thrombocytopenia.1.5 lakhs to 4.5 lakhs platelets/μ L count is the normal in blood. Patient will be asymptomatic many times. bruising, purpura, petechiae, bleeding from the gums, nose are the symptoms develop in some patients. When the platelet count goes less than 5000/mm3there will be bleeding in the brain and gastrointestinal system and causes life risk symptoms. Thrombocytopenia is caused by virus, bacterial and also by protozoal infection with or without DIC. Febrile thrombocytopenia is also caused by malaria, dengue, leptospirosis, septic infection, scrub typus, rickettsial infection and meningococcal infection.

In monsoon and post monsoon period febrile thrombocytopenia cases comes to outpatient department. Sometimes some patients will be admitted in IMCU with multi organ damage which results in high mortality and morbidity of the patients with febrile thrombocytopenia. Some patients recover by self from the infection but to prevent the deadly complication patient is monitored 24 hours.

If the identification is earlier and the treatment in early stage reduces the mortality and morbidity in the patients. As the number of cases were increasing day by day the factors are important in the prognosis of the patients.so this was done to study about the prognostic factors in patients

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presenting to the hospital with fever thrombocytopenia to tertiary hospital which is linked Tamilnadu medical college.

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2.REVIEW OFLITERATURE FEVERWITH THROMBOCYTOPENIA

For seven to ten days ,In circulation platelets will be seen, in the spleen some platelets will present and some of them in the circulation. The range of normal platelet count is 70,000 to 4.5 lakhs in the neonates and after that 1.5 lakhsto4 lakhs/mm3. the increase or decrease in the platelet counts are found by the automatic instrument which detect the change.

If the platelet is <80thousand /mm3 in the neonate and<1.5 lakhs /mm3 is diagnosed to be thrombocytopenia. There are many number of causes and mechanism for thrombocytopenia. Hematopoiesis will be affected and there will be decreased production in platelets by infection.

Destruction due to immune mediated may be due to acute or chronic which can occur in all infections due to viral (e.g.,infection due to CMV, infection due to EBV, infection due to HIV, rubella infection, and hepatitis type Band type C)and may be due to infections which is subacute (e.g.,leptospirosis, endocarditis and syphilis).

Immune-mediated destruction causes ITP,it is followed by viral infection, which results in thrombocytopenia and muco-cutaneous bleeding among healthy adults.

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Non-immunologically profound thrombocytopenia and DIC is caused by acute viral or bacterial infection. Thrombocytopenia is also caused by plasmodium, anaplasma and rickettsia which causes acute infection. s.aureus exotoxin and enteric bacilli endotoxin (bacterial toxins)causes thrombocytopenia without increase in number of bacteria.

In hemolytic uremic syndrome thrombocytopenia is associated with E coli organisms which contains shiga like toxin which also causes micro-angiopathic thrombosis. Bone marrow suppressant action and peripheral destruction action is due to systemic viral illness which occurs after the decline of thrombocytopenia range from 80 thousand to 1.5 lakhs

Immune-Mediated Destruction

*Idiopathic thrombocytopenic purpura

*Malignant diseases

*Drugs (sulfa, ampicillin, rifampin, quinine, and multiple non antimicrobial agents)

*Infection (especially Epstein–Barr virus, cytomegalovirus, human immunodeficiency virus, hepatitis B and-C, congenital syphilis, toxoplasmosis, viral infections, subacute endocarditis)

*Vaccines

*Autoimmune diseases

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Nonimmune Destruction

*Disseminated intravascular coagulation

*Septicemia

*Viral, rickettsial, fungal infection

*Hemolytic uremic syndrome

*Bacterial toxin–mediated syndromes

*Malaria

*Organ transplant rejection

*Cyanotic congenital heart disease Pseudothrombocytopenia

-Aggregation of platelets not counted by electronic cell analyzers

PATHOPHYSIOLOGY:

Thrombocytopenia resultsfrom4 processes.

# Accelerated platelet destruction

# Deficient platelet production

# Abnormal distribution or pooling of platelets within the body.

# Artifactual Thrombocytopenia

Second count should be always done to confirm the low platelet count which is lower than normal. Thrombocytopenia should also be confirmed by after examining the blood film thrombocytopenia should be confirmed. For accurate results electronic particle counter are widely used now.

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PATHOPHYSIOLOGICCLASSIFICATIONOF THROMBOCYTOPENIA

a) Artifactual Thrombocytopenia b) Increased platelet destruction

i) Immunologic process ii) Non-immunologic process c) Decreased platelet production d) Abnormal platelet pooling.

ETIOLOGY:

Common causes of fever with thrombocytopenia in India of infectious etiology are

*Dengue

*Malaria

*Enteric fever

*Urinary tract infection

*Sepsis

*Leptospirosis

*Scrub typhus

Dengue

Aedes species Mosquitoes bites the human and transmit the dengue virus. Dengue virus is of four types they are DENV-TYPE 1,DENV-

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TYPE 2,DENV-TYPE3 and DENV-TYPE 4,most commonly Aedes aegypti and A.albopictus. infecting dengue virus produces immunity which is life long which is specific. Heterotypic immunity which is cross protective is mostly short term. 3 to10 days is the dengue usual incubation period. infections caused by dengue virus about 75% produces febrile illness which is mild and asymptomatic.

Dengue only with fever, dengue with hemorrhagic fever, and dengue with shock syndrome are the overlapping presentation of the dengue . only dengue, dengue with warning signs, and severe dengue which are the modified clinical classification for the dengue guidelines given by World Health Organization.

Mostly dengue is acute presentation and self limiting disease in which the patient recovers within 7 days without complications.. Leakage from the plasma, presentation with shock or fluid accumulation with respiratory distress in which there is accumulation of fluid, serious hemorrhages and severe organ failure are manifestations of the dengue which is about 7% in the endemic areas. Treatment should be given correctly or else 5% case mortality seen in the study. In severe dengue DENGUE VIRUS has association with the secondary infection.

Hepatitis, encephalitis and myocarditis are the rarest dengue manifestation. febrile, convalescent and critical are the three phases of dengue clinical course divided by guidelines given currently by the WHO

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HEALTH ORGANISATION.There will be high-grade fever in the acute febrile phase of dengue. In dengue primary symptoms are myalgia, headache, retro-orbital pain, vomiting, nausea Other symptoms include maculopapular rash, arthralgia, conjunctival congestion and facial flushing.

After inflating the cuff of blood pressure (appearance of petechiae more than 10 skin patch of 2.5cm square) denotes tourniquet test positive in many of the dengue patients, about25% of the patient have epistaxis ,gum bleeding are the hemorrhagic manifestations seen in 25% of the dengue patients. Common laboratory abnormalities include thrombocytopenia, hyponatremia, leukopenia and increased SGOT and SGPT enzymes are the common labarotory abnormalities.

After 2 to 7 days of onset of the illness dengue critical phase commences in 24 to 48 hrs. During this time patient recovers from the illness and most of the patients improve. Warning signs of severe dengue are

1. Decreasing platelet count 2. Restlessness

3. Extravascular fluid accumulation 4. Increasing hematocrit

5. Restlessness 6. Lethargy

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7. Hepatomegaly 8. Abdominal pain

9. Severe mucosal bleeding.

10.In most of the patients there will be presence of ascites and pleural effusion in the USG ABDOMEN or chest x ray

If the patient worsen due to shock due to plasma leakage there will be narrowed pulse pressure and DIC(disseminated intravascular coagulation).in patients without shock or in the absence of plasma leakage there will be presence of severe hemorrhage and critical multi organ dysfunction.

IV fluids are given in a severe dengue patients and managed according to latest guidelines given by world health organization(WHO). by early detection and effective fluid correction mortality rate of the dengue is reduced to <0.4%.within48hours resolving of the dengue critical phase occurs, and patients goes to the next phase. In convalescent phase there will be reabsorption of extravascular fluid in next 2 to 3 days with increased frequency of urine. Erythematous rash is developed in some patients with bradycardia, or abnormalities in the electrocardiography when excess fluid is administered there will CCF(congestive cardiac failure) and pulmonary edema.

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Dengue patients without warning signs can be treated as outpatients by advising them to take rest, monitoring vitals, giving importance to hydration, treating with paracetamol for pain. to prevent the bleeding risk drugs like asprin and other NSAIDS (non steroidal anti-inflammatory drugs should be avoided.

The transmission of dengue infection from mother to fetus is not proved. Congenital infection of dengue is also not proved. But some research shows increased risk of preterm birth and low birth weight baby in mother having dengue infection.in congenital dengue neonate clinically presents with febrile thrombocytopenia, pleural effusions, shock and severe hemorrhage.

MALARIA:

The infecting species of Plasmodium infecting species and host of immune specific malaria determines the malaria clinical features .symptomatic illness is also developed in a non immune people who moved from endemic area. Infections caused by the four species which naturally affect humans are less severe than the infection caused by the p.falciparum infection. in malaria there will be cyclical occurrence of sudden coldness followed by shivering and then fever and sweating occurring every two days (tertian fever) in p.vivax and p.ovale infections, and every three days(quartan fever) for p.malariae. Which lasts from ten

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to twelve hours. Special features of malaria are fever with chills and rigor, fever with seizures and profuse sweating headache, body pain, joint pain, easy fatigability are the nonspecific symptoms of malaria fever.

Gastrointestinaltract symptoms, including loose stools, nausea, abdominal pain are the GIT(gastrointestinaltract) symptoms of malaria. Although prostrated during febrile episodes, patients will not have any symptoms between the episodes and symptoms during the episodes of fever. patients who came from the endemic area are highly suspected to have malaria.

In patient with low levels of parasitemia clinical symptoms will be seen in non immune patients. Three samples of thick &thin blood smears are taken separately by interval of 12 to 24 hours to confirm the malaria diagnosis. infections of the p.Falciparum cause cerebral affects results in increased mortality and morbidity rate.in malarial fever when the patient develops confusion and delirium indicates that the patient needs urgent treatment and imcu care. Patient get worsens to coma. Generalized seizures, and symmetric UMN dysfunction, focal neurologic signs are not commonly seen in malarial patients. As the cause of encephalopathy is metabolic the patients responds to anti malaria treatment and the patient also recovers from the CNS manifestations. Seizures, coma, hypoglycemia are the risk factors for the CNS manifestations, ICT(intracranial tension) and neurological sequale in malarial patients.

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The increased mortality rate is due to respiratory failure and renal failure is increased in p.falciparum infected patients who have respiratory failure and renal failure. Respiratory failure does not indicate the poor prognosis, It indicate the decrease in parasitemia by effective treatment .

ATN (Acute tubular necrosis) is the commonest presentation of renal failure ,in this patient will have low BP and hypovolemia.. it is a common complication seen in adults who are nonimmune.

In chronic disease increased parasitemia (infected RBC increased>5%) is seen. It affects the low immunity people. Low BP, low sugar &metabolic acidosis are the characteristic features of the p.Falciparum infections in non immunity people. parasitemia &

association of cytokine alteration are the signs with gram negative sepsis causing bacteria along with GIT (gastrointestinaltract) symptoms.

Particularly when we are treating the patients with quinine or quinidine therapy we should watch for hypoglycemia and treat it effectively.

Anemia is an expected consequence of malaria, especially in patients with increased parasitemia anemia is a complication in malaria. Hemolysis occurs which is due to parasitosis resulting in the hypersplenism in which RBC are destructed and erythropoiesis abnormalities, hemolysis are the etiopathological factors resulting in anemia. Thrombocytopenia is extremely common in malaria, including very low platelet counts, bleeding manifestation due to low platelet count is rare in malaria but

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thrombocytopenia is common. Usually coagulopathy is not seen in malaria but it is seen in infection of P. falciparum in nonimmune people. Septic shock–like syndrome is seen in algid malaria.

In black water fever there will be hemolysis with hemoglobinuria, which is seen in non immune people with hyperparasitemia. This condition is seen in people living in endemic areas who are exposed to prolonged quinine intake, G6PD(glucose-6-phosphate dehydrogenase) and patient on antimalarial drugs .

In acute illness malarial patients presents with complications, But the patient get recovers from CNS(central nervous system),renal and respiratory failure.

Typically Giemsa- based stains is used for the hematological stain to the malarial parasite in blood smear. The thick film preparation is the more sensitive technique is identifying the parasite in thick film smear,But itis more difficult to interpret by inexperienced examiners feels difficult to identify in in thick smear. It can be identified in a thin smear.

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Thrombocytopenia which is usually seen in the malaria in which the platelet count will be less than 50 thousand/mm3 .meningitis is the differential diagnosis for cerebral malaria .lumbar puncture is done in which the CSF contain elevated protein and lymphocytic pleocytosis. in malaria there will be dehydration, vomiting, medical renal disease which is the cause for hyponatremia and metabolic acidosis in severe malaria.

We have to watch for Hypoglycemia in treating the patient with quinidine .In high fever proteinuria is abnormal in the urinalysis report. if hemolysis occurred there will be presence of hemoglobinuria in urinalysis.

If there is presence of RBC shows the association of glomerulonephritis.

Elevation of liver enzymes and increased bilirubin are seen hepatic failure is not common so we have to look for other causes.

LEPTOSPIROSIS:

Liver &kidney are the organs infected by leptospira organisms and they cause abnormalities in hepatocellular function which ultimately results in jaundice in which there will be no necrosis.Hemorrhagic vasculitis & renal failure are also caused by the bacteria. in the

“septicemic” phase of the leptospirosis signs and symptoms are caused by organism direct effect antigen-antibody complexes will be seen in immune phase.

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The incubation period will be in the range of7–14days .but for some patients it will be short for 2 days and also extend to 25 days in some patients .there are two phases one is initial “septicemic” phase and other is the “immune” phase.. some patients presents with icteric form which is more common, some patients with anicteric form which is less common.

Anicteric Leptospirosis

Symptoms are high grade fever, projectile vomiting, body pain, headache. Patients also presents with the symptoms of abdominal pain, diarrhea, easy fatigability, anorexia, and conjunctival congestion. Patients rarely presents with the circulatory collapse. During this phase of illness, organisms will be seen in the blood and CSF(cerebrospinal fluid) during this phase. symptoms usually last 4 to 7 days and during this phase illness spontaneously resolves in 4 to 7 days .

1 to 3 days later immunologic phase illness begins with low-grade or absence of fever. During this phase, headache, conjunctival congestion, rash, bodyache, are seen during this phase. Other symptoms like abdominal pain, nausea, vomiting and severe headache with nuchal rigidity is also present. aseptic meningitis presentation is also seen for many days,but they can also persist in some patient for 2 to 3 weeks. GBS(Guillain-Barré syndrome),mononeuropathy,polyneuropathy&encephalitis are the nervous

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system disease which are immune mediated clinical manifestation of the disease.

Pus in urine, blood in urine & protein in urine are the clinical manifestation of the Interstitial nephritis which is common. Some Patients have right hypochondrial pain and acholecystitis with gallbladder hydrops.

Pulmonary manifestation is also present. Leptospirosis rash is mediated by immune & it can be macular, maculopapular rash, urticarial rash, petechial rash or purpuric rash. The infectious and immune phases which is infectious form of anicteric leptospirosis recovers in 2 weeks from the intiation of symptoms.

Icteric Leptospirosis (Weil Syndrome)

multiple serotypes ofLeptospira causes icteric form of leptospirosis which is severe form also termed as weil syndrome. 5%to10% is the mortality rate of the leptospirosis anicteric form in the early phase.

Jaundice bleeding manifestation & azotemia are the hallmarks features of the weils syndrome which is seen in 4to6daysafterthe intiation of symptoms and progress in the second week illness. Fever lasting for 2–

3weeks which is persistant in severe leptospirosis catastropic manifestation is the pulmonary hemorrhage which is often fatal. Although hepatomegaly, hepatocellular injury, and jaundice are prominent features of in Weil syndrome prominent features are liver enlargement, injury to

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hepatocellular &jaundice which does not leads to necrosis & frank hepatic failure .

renal failure is seen in two forms of leptospirosis. renal failure&

ATN(acute tubular necrosis) is due to shock & hemoglobinemia from hemolysis is by bacterial toxicity to the renal tubules. As the technology has improved in recent years the survival rate was improved. Renal impairement is not reversible in all cases.

Cardiac abnormalities is rare, though some patients have nonspecific abnormalities in ECG like first degree heart block at the time of first week of the illness. congestive heart failure & sudden cardiovascular collapse are rarely seen inpatients of Weil syndrome.

Laboratory Findings and Diagnosis

abnormalities in the labarotory investigation depends on the illness phase, severity and systemic involvement.. None isspecific. Leukocytosis

& neutrophilia are seen in weil syndrome, at the time illness in early phase.

Anemia is not commonly seen in anicteric form of leptospirosis but if present it will be severe in Weil syndrome.

In anicteric leptospirosis renal parameters ,hepatic enzymes are elevated but it is seen more in weil syndrome. During the immune phase patients of leptospirosis clinically presents with meningeal signs which is

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seen in one half of the of the patients, in CSF (cerebrospinalfluid) predominent neutrophils with pleocytosis, elevated or normal protein and the normal glucose. White blood cells(WBC), red blood cells(RBC), cellular casts and protein are seen in the early phase of the illness.

Leptospira absence in the fluid or tissue confirms the diagnosis of recovery.rise in anti-leptospiral antibodies rise in agglutination test is seen in acute and convalescents era In a patient with illness clinically.

Antileptospiral antibodies of greater than 1:100 seen in microscopic agglutination test confirms the compatible illness for the diagnosis or a macroscopic agglutination test is positive for the diagnosis. result. in routine light microscopy we cannot visualize the leptospira organism ; in urine or tissue specimens by the use of fluorescent antibody technique or modified silver stain we can easily visualize the organism. Dark field microscopy are rarely used to visualize the leptospira if the organism density is high.

Treatment

Generally leptospirosis is a self-limiting disease. Even though the Treatment is started later in severe infection ,potentially it is beneficial.

Jarisch-Herxheimer reaction occur frequently shows the effect of treatment. for every6hours aqueous pencillin G of 1.5 million units IV or IM is given..inj Ceftriaxone of dose 2g/day IV can also be given

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alternative. Less seriously ill patients can be treated with capsule doxycycline 100mg PO twice a day or amoxicillin of dose 500mg PO thrice a day. Azithromycin 250mg PO once or twice a week is given as chemoprophylaxis.

URINARYTRACTINFECTION

A common cause of fever is UTI and in which renal parenchymal damage may present& loss of function. Renal damage in UTI can be reduced by prevention and treatment by rapid diagnosis.

Etiologic Agents

The most common bacteria that cause UTI is caused commonly by gram-negative Enterobacteriaceae E.coli and the other bacteria causing UTI are proteus, Klebsiella, Pseudomonas, &Enterobacter species.

Infection is facilitated by O- antigen in cell wall of extaintestinal E coli and uropathogenic Ecoli are the serotypes of E coli.

Staphylococcus aureus rarely causes UTI symptoms and its isolation in urine suggest primary infection,

Pathogenesis

In UTI first the bacterial adherence to epithelial cells host through the fecal-perineal-urethral route bacteria ascent in a retrograde fashion along

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the urinary tract. Bacterial virulence does not cause renal scarring, Pyelonephritis, Parenchymal or functional loss.

UTI is caused when urethral defense is overcome by urethral defense. Epithelial shedding, urethral washout and paraurethral glandular secretion are the urethral defense mechanism done to prevent the urinary tract infection.

Mannose-resistant hemagglutination & P blood group specific adhesion are two main markers of E.coli. type 1 pili of the bacteria attaches to the uroepithelial cell and molecular interaction is intiated by the fimbria and then there will be bacterial uptake into umbrella cells which is seen on the surface of the bladder. Host immunity, vesicouretral reflex, impaired ureteral peristalisis & organism-specific uropathogenicity affect the retrograde ascent of bacteria from bladder to kidney in the bladder.

Clinical Manifestations

UTI should be the differential diagnosis in adults who have fever with chills & rigor .patients complaints of flank pain along with fever, chills& rigor, nausea and vomiting. Other symptoms can include dysuria, increased frequency, urgency and incontinence are the other symptoms.

Sexually transmitted infection and both UTI should be evaluated in patients with lower urinary tract symptoms. On palpation tenderness present in the suprapubic and flank region.

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LaboratoryFindings UrinarySpecimens

To diagnose the infection urine sample should not be uncontaminated.In urine collection there are various methods. One Of the reliable method of urine collection is suprapubic aspiration as it escapes from the contamination by urethral and periurethral pathways. Although bacterial presence confirms the diagnosis of UTI ,doctors are not following this technique as it is a invasive technique. So urethral catheterization is done in a sterile method, sample can be taken for urine culture and sensitivity risks for catheterization include urethral trauma and the infection by introduction of bacteria into the bladder are the risks of catheterisation.

In circumcised male patients and female who give specimen by retracting labial tissue are more reliable and less chance of contamination. urine collected from the urinary bag are the least reliable method and when the culture is negative it is useful.Perineal and rectal flora will be seen in a bagged urine even in a cleaned skin surrounding .

Urinalysis

Diagnosis of UTI include

1. pyuria, defined as more than 5white blood cells(WBCs) per high power field(HPF)in a centrifuged specimen

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2. Any bacteria visualized under high power in an unstained centrifuged urinary sediment(×40)

3. Presence of urinary leukocyte esterase and 4. Positive test for urinary nitrite

Degradation of wbcs produces leukocyte esterase in the urine. The urinary nitrite test measures dietary nitrates reduced to nitrates by gram negative Enterobacteriaceae reduces dietary nitrates to nitrates which is confirmed by urinary nitrite test. This test cannot be done in Gram- positive bacteria, pseudomonas species, and yeast which do not reduce the dietary nitrates.

Positive predictive value of 100% is approached by positive nitrite test, presence of leukocyte esterase and bacterial visualization in microscope in a appropriatly collected urine specimen is given specific treatment for UTI.

Urine Culture

Gold standard of diagnosis for UTI is the quantitative urine culture.

In UTI there will be growthof100,000CFUs/mL in a urine specimen . Guidelinesfrom2011suggestthatthe presence of pyuria plus bacterial growth of 50,000CFUs/mL or more is sufficient for UTI diagnosis guidelines given in 2011 suggest the presence of pus and bacterial growth of 50 thousand CFUs/ m L confirms the diagnosis. The presence of <10

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thousand CFUs/mL in urine sample from suprapubic aspiration is associated with infection.

Serum Tests

Although urinary culture is the standard for diagnosing UTI ,urinary culture is the standard test, some other tests are also done to Assist the severity of infection is also done. in severe bacterial infection ESR(erythrocyte sedimentation rate) & CRP(C reactive protein) are elevated.In sepsis calcitonin the inactive precursor of procalcitonin is elevated.

Management

Antimicrobial Treatment

Nitrofurantoin, ampicillin, and the cephalosporin are considered relatively safe in early pregnancy. Sulfonamides should be avoided in the first trimester because of possible teratogenic effects and near term because of possible role in the development of kernicterus.

fluoroquinolones are avoided because of possible adverse effects on fetal cartilage development. A 7 to 14 day course of a fluoroquinolone or TMP –SMX is recommended if the uropathogen is susceptible. Therapy for complicated urinary tract infection must be individualized and guided by urine culture report.

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SCRUB TYPHUS:

chigger (larval mite) bites transmits scrub typus and antigenically involved in diverse strains of Orientiatsutsugamushi. O.Tsutsugamushi is the causative agent of tsutsugamamushi fever or scrub typhus. It also infects macrophages and cardiac myocytes.

PATHOGENESIS

After the infection of vascular endothelium cells stimulation of pathogenic process , which is associated to the presence of perivascular inflammation and disseminated vasculitis. Significant vascular leakage is caused by the immune mediated inflammation which cause infection. Brain and lungs are the most common organ involved due to vascular compromise and end organ injury, as like other vasculo tropic rickettsioses.

CLINICAL MANIFESTATIONS ANDLABORATORYFINDINGS Fever will be lasting for 9-11 days ranging 1 to 30 days before going to hospital. Liver enlargement, spleen enlargement and localized or generalized lymphadenopathy present. GI symptoms, including abdominal pain, vomiting, and diarrhea , nausea, vomiting and abdominal pain are the GI symptoms present. A maculopapular type of rash is seen in<30%;both it can be absent sometimes. At the site of chigger bite there is a single painless eschar with an erythematous rim seen in 5-70% cases.

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Hemophagocytic lymphohistiocytosisis also seen. Thrombocytopenia is seen in 25-35% with normal Leukocyte and platelet counts. About 40% of cases leukocytosis is reported.

DIAGNOSIS

Indirect fluorescent antibody or immunoperoxidase assays are the serologic tests done to confirm the diagnosis which is also based on clinical suspicion. PCR(Polymerase chain reaction) are not the highly sensitive test , and not followed widely.

TREATMENT ANDSUPPORTIVE CARE

treatment for scrub typhus is doxycycline 100mg bid orally for 7-15 days. Alternative regimens include azithromycin 500mg orally for 3 days or chloramphenicol 500mg qid orally for 7-15 days.

SEPSIS

It is caused by the bacteria such as E.coli & groupB Streptococcus.,Listeria monocytogenes, enterococci & Staphaureus (including methicillin resistant Staphaureus[MRSA]), Streptococcus pneumoniae are the other common organism involved in sepsis.S.aureus and Streptococcus pyogenes are the other organism causing sepsis, and also causes TSS(toxic shock syndrome)Species of Salmonella and rickettsiae are also the causative of sepsis. Sepsis is also caused by Malaria and dengue fever.

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Pathophysiology

In multiple organs adherence of platelets to activated endothelium occurs in sepsis. After adhesion platelet may go back to the circulation or goes for irreversible aggregation with metamorphosis.

Enhancement of platelet reactivity and adhesivity causes sepsis induced thrombocytopenia by inflammatory mediators and bacterial endotoxins.

Cytopenia in sepsis occurs by reticuloendothelial system which phagocytosis the platlets.it is also contributed by immune mechanism.in 30% of the IMCU patients nonspecific platelet associating antibodies are detected.it is directed against the glycoprotein 2b/3a .they are involved in the pathogenesis of immune mediated thrombocytopenic purpura.

Hemophagocytic histiocytes are seen in a bone marrow of sepsis patients.

Elevation of macrophages, CSF(colony stimulated ) is associated with the presence of multiorgan dysfunction.GP2b/3a and GP 1b/9 which are the antibodies to specific antiplatelet antigen are detected in sepsis patients.in acute phase there will be increased platelet count so called thrombocytosis occurs.in medical ICU 25% of the cases have thrombocytopenia.40% of the cases have thrombocytopenia.36% to 60% is the incidence of thrombocytopenia. Patient on heparin theraphy have thrombocytopenia as a complication. Patient who have underwent a complicated surgery have dilutional thrombocytopenia which is also seen in trauma patients and

(36)

cancer patients. In ITP(immune thrombocytopenic purpura) low platlet count is seen.

Inspite of antimicrobial therapy and intensive care, organ dysfunction and thrombotic complications occurs which results in increased morbidity and death.

Clinical manifestations

There will be variation in patient developing sepsis from one patient to other patient. some patient will be normothermic and some patient will be hypothermic, fever will be absent in elderly patients, neonates, chronic alcoholism and patients with uremia. Early sign in the septic response is hyperventilation causing respiratory alkalosis. The other manifestation of encephalopathy like confusion, disorientation develop early specifically in elderly and in patients already having neurology impairement.

Gastrointestinal manifestations such as vomiting ,nausea and diarrrhea are the gastrointestinal manifestation which suggest acute gastroenteritis. upper gastrointestinal bleeding is also caused by stress ulceration. Due to increased glycolysis and impaired clearance of pyruvate and lactate by kidneys and liver rise in blood lactate levels occurs early .blood glucose concentration often increase in blood glucose level is seen, in diabetes patients hypoglycemia is produced due to impaired gluconeogenesis and excess insulin release.

(37)

Diagnosis

In sepsis there is no specific test to diagnose. fever, tachypnea ,hypothermia, tachycardia and leukocytosis or leukopenia are the sensitive findings in infection for the diagnosis of sepsis. altered mental status, low platelet count, an increased blood lactate level, respiratory alkalosis & hypotension is also the clinical features for the diagnosis.

Definitive etiologic diagnosis requires identification of the causative microorganism is identified from blood or from the local site of infection.at least two blood samples are taken from two different sites for blood culture. If the blood culture is negative, it not only signifies the absence of bacteria, This also shows prior administration of antibiotics administration some organism grows slow and some are fastidious, the presence of slow growing or fastidious organism ,or the microbial invasion absence in the blood stream.

Management

Antimicrobial Therapy

Empiric therapy should be started earlier in suspected cases of sepsis. And it should be against the pathogens causing infection. antibody regimen is selected by community, immune status of the individual, and tissue penetration and compartments. Vancomycin is also included in the empiric regimen if the clinical presentation is associated with infection by

(38)

staphylococcus. The organism should be evaluated for ESBL production if the organism is E.COLI OR KLEBSIELLA SPECIES (gram negative bacteria).

The treatment of choice is carbapenam who is having serious infection. Infections caused by carbapenem resistant Enterobacteriaceae causes infection which is increasing worldwide and is also seen in adult populations.

Enteric Fever

Salmonella strains is associated with enteric fever (typoid fever). The clinical features of enteric fever with Salmonella Typhi or Salmonella Paratyphi causing enteric fever are indistinguishable. Fever in the first week of illness, which is non-remitting and clinically presents with symptoms such as myalgia, headache, malaise & abdominal pain .stepladder pattern is seen.

Hepatosplenomegaly, rosespots headache replaced by stupor is seen in the second week may be seen. Relative bradycardia is seen in typhoid fever .During the third to fourth week of fever, Intestinal hemorrhage &

perforation occurs commonly in third to fourth week of fever ;remitting type of fever begins in morning, and fever spikes declines gradually.

Meningitis, shock, Myocarditis, and pneumonia are the complications of the course of the disease .

(39)

Patients will be having bloody diarrhea with blood and leukocytes in fecal in the earlier weeks, but in some patients diarrhea is not the presentation till third week. Occasionally, resolution is not seen till6weeks.reccurance is also seen.

After the first week of illness death occurs due to CNS involvement.

Perforation and intestinal hemorrhage.

DIAGNOSIS:

For the diagnosis of typhoid fever blood culture is the laboratory investigation done. the blood volume from the sample determines the blood culture sensitivity.

Culture of bone marrow culture is the more sensitive test,but it is not done frequently. In patients with persistent fever bone marrow culture is useful for the diagnosis., CSF(cerebrospinal fluid)&biopsy specimen are cultured to identify the salmonella serotypes.

TREATMENT:

Inj.Ceftriaxone 2g/d IV is given as the empirical treatment for enteric fever for 10-14 days. For fully susceptible patients the optimal treatment is 500mg bid (PO) or 400mg q12h(IV) for 5-7 days.

Azithromycin,amoxicillin,chloramphenicol,trimethoprim-sulfamethoxazole can also be used in fully susceptible patients. multidrug-resistant patients and quinolone-resistant are treated with inj.ceftriaxone. Compared to

(40)

fluroquinolones Azithromycin is associated with less treatment failure and the duration of stay in the hospital is also reduced.

In patients with shock and obtundation dexamethasone in initial dose of 3mg/kg followed by eight dose of 1mg/kg for every 6 hours with chloramphenicol is associated with lower mortality.

If patients develop intestinal perforation surgery is the treatment of choice along with the broad-spectrum antimicrobial therapy.

(41)

3.STUDYJUSTIFICATION

Fever with thrombocytopenia is one of the leading cause of mortality and morbidity in adults. There are various infectious causes for fever with thrombocytopenia including deadly dengue fever and bacterial sepsis. The admission rate of fever with thrombocytopenia in tertiary care hospital remains high in previous 5 years. The mortality and morbidity also remains high.

Various studies have showed that there are many prognostic factors which are very useful in predicting the outcome. These factors also alert the treating physician in taking many crucial decisions like whether to treat the case as opd or to admit and treat aggressively. This study includes all the patients above 12yrsadmitted as fever with thrombocytopenia and aims to identify various clinical, laboratory parameters for predicting the outcome in tertiary care centre hospital.

(42)

4.AIMOFTHE STUDY

The study of clinical and laboratory parameters in predicting the outcome of patients with fever with thrombocytopenia above 12yrs admitted in Tirunelveli Medical College during the time period of 2018 and 2019.

Following parameters at admission are considered to predict the outcome among the study group.

1. Age 2. Sex 3. Locality 4. Day of fever 5. General condition 6. Respiratory distress 7. Abdominal distension 8. Hepatomegaly

9. Dehydration 10.Total count 11.Platelet count 12.PCV

13.RFT

14.Liver enzymes

(43)

15.Warning symptoms 16.Serum proteins 17.Coagulation profile 18.Ascites

19.Pleural effusion

20.Serology & Culture sensitivity

(44)

5.MATERIALS ANDMETHODS STUDYCENTRE

Our study was conducted at Department of medicine, Tirunelveli Medical College Hospital

STUDYGROUP:

All cases of fever with thrombocytopenia age more than 12yrs admitted during the period of 2018 and 2019 in medicine Department of Tirunelveli Medical College Hospital.

STUDYDESIGN:

Prospective observational study STUDYDURATION:

January2018toJune2019

INCLUSIONCRITERIA:

All the patients above 12years presenting with the complaints of fever (>99.9degree F) with thrombocytopenia (lessthan1,50,000/μL).

EXCLUSIONCRITERIA:

1) Patient presenting with thrombocytopenia without fever.

2) Diagnosed case of immune thrombocytopenic purpura.

3) Patient with thrombocytopenia already diagnosed to have hematological disorder/malignancy or on treatment with chemotherapy and other immunosuppressive agent.

(45)

4) Diagnosed cases of platelet disorder and dysfunction.

5) Patients on treatment with antiplatelet drugs and other drugs causing thrombocytopenia.

6) Patients with cirrhosis and chronic liver disease 6.METHADOLOGY

After getting consent, detailed history, clinical details and Investigations were collected and entered in the proforma. It includes age, sex, locality.

History regarding day of fever, warning symptoms including abdominal pain, vomiting, hemetemesis, reduced urine output, passing black coloured stools are recorded at the time of admission.

Clinical features includes general condition, respiratory distress (tachypnea, retractions), abdominal distension, hepatomegaly, dehydration (dry oral cavity, increased thirst) are recorded at the time of admission.

Blood investigations including total count (normal:4000-10000, leukopenia<4000, leukocytosis>10000), platelet count, PCV, RFT (normal Urea <40, creatinine0.5-0.8), Liver enzymes (normal AST<40, ALT<40, ALP <150), serum proteins (normal Total protein6, serumalbumin4, serumglobulin2), coagulation profile (normal PT16, APTT36, INR<1.5), Serology & Culture sensitivity are recorded at the time of admission.

(46)

Chestx-ray, Ultra sonogram abdomen and chest findings including acites, pleural effusion are also recorded.

Outcome was assessed as morbidity in the form of only fever, fever with bleeding and hemorrhagic fever with shock.

(47)

7.STATISTICAL ANALYSIS

Data collected and recorded in the proforma during the whole study period were entered in Microsoft Excel Sheet and analysed value calculated to identify whether various risk factors for morbidity and mortality for fever with thrombocytopenia are statistically significant.

(48)

8.RESULTS

TOTAL NO OF CASES:100

OUTCOME NO OF CASES TOTAL %

OF 62 62%

HFWOS 15 15%

HFWS 23 23%

OF-ONLY FEVER HFWOS-HEMORRHAGIC FEVER WITHOUT SHOCK HFWS-HEMORRHAGIC FEVER WITH SHOCK

ONLY FEVER 62%

FEVER WITHOUT SHOCK

15%

FEVER WITH SHOCK

23%

SIGNIFICANCE

(49)

AGE DISTRIBUTION

AGE NO OF CASES TOTAL %

< 30 YRS 60 60%

> 30 YRS 40 40%

60%

40%

AGE DISTRIBUTION

< 30 YRS

> 30 YRS

(50)

AGE OF HFWOS HFWS TOTAL

< 30 YRS 36 9 15 60

> 30 YRS 26 6 8 40

KRUSKAL WALLIS TEST P VALUE - 0.836

NON SIGNIFICANT

36 9 15

26 6 8

O N L Y F E V E R ( N = 6 2 ) F E V E R W I T H O U T S H O C K

( N = 1 5 ) F E V E R W I T H S H O C K ( N = 2 3 )

AGE AND ITS SIGNIFICANCE

< 30 YRS > 30 YRS

(51)

SEX DISTRIBUTION

SEX NO OF CASES TOTAL %

MALE 57 57%

FEMALE 43 43%

among admission 57% were male patients 43% were female patients

57%

43%

SEX DISTRIBUTION

MALE FEMALE

(52)

SEX OF HFWOS HFWS TOTAL

MALE 32 10 15 57

FEMALE 30 5 8 43

NON SIGNIFICANT

32 10 15

30 5 8

SEX AND ITS SIGNIFICANCE

MALE FEMALE

(53)

LOCALITY

LOCALITY NO OF CASES TOTAL%

RURAL 80 80%

URBAN 20 20%

80% of the admitted cases came from rural area.20% belonged to urban area.

RURAL 80%

URBAN 20%

LOCALITY

RURAL URBAN

(54)

LOCALITY OF HFWOS HFWS TOTAL

RURAL 51 13 16 80

URBAN 11 2 7 20

KRUSKAL WALLIS TEST P VALUE -0.337

NON SIGNIFICANT

51

13 16

11

2 7

0 10 20 30 40 50 60

ONLY FEVER (N=62) FEVER WITHOUT SHOCK

(N=15) FEVER WITH SHOCK (N=23)

LOCALITY AND ITS SIGNIFICANCE

RURAL URBAN

(55)

DAY OF FEVER

DAY OF FEVER NO OF CASES TOTAL %

< 4 DAYS 42 42%

> 4 DAYS 58 58%

patients admitted for 4 days fever are 42% .patients admitted for more than 5 days are 58%

42%

58%

DAY OF FEVER

< 4 DAYS

> 4 DAYS

(56)

DAY OF FEVER OF HFWOS HFWS TOTAL

< 4 DAYS 32 5 5 42

> 4 DAYS 30 10 18 58

SIGNIFICANT

among 100 cases admittted , more than 4days fever cases are 58%.

In this 58% , 30% of the patients developed only fever,10% patients had hemorrhagic fever without shock. remaining 18% had hemorrhagic fever with shock with 0.035 pvalue. It shows the significant association of day of fever with outcome.

0 5 10 15 20 25 30 35

O N L Y F E V E R ( N = 6 2 ) F E V E R W I T H O U T

S H O C K ( N = 1 5 ) F E V E R W I T H S H O C K ( N = 2 3 )

DAY OF FEVER & ITS SIGNIFICANCE

< 4 DAYS

> 4 DAYS

(57)

GENERAL CONDITION

GENERAL CONDITION NO OF CASES TOTAL%

CONSCIOUS 68 68%

DROWSY 32 32%

In admissions patient with normal general condition is seen in 68%.

68%

32%

GENERAL CONDITION

CONSCIOUS DROWSY

(58)

GENERAL CONDITION OF HFWOS HFWS TOTAL

CONSCIOUS 60 7 1 68

DROWSY 2 8 22 32

SIGNIFICANT

OF-ONLY FEVER HFWOS-HEMORRRHAGIC FEVER WITHOUT SHOCK HFWS-HEMORRHAGIC FEVER WITH SHOCK

among 100 patients admitted , general condition of the patients normal in 68%. In this 68% , 60% of the patients developed only fever,7%

patients had hemorrhagic fever without shock.remaining 1% had hemorrhagic fever with shock with 0.01 pvalue. It shows the significant association of general condition of the patients with outcome.

0 10 20 30 40 50 60

ONLY FEVER (N=62) FEVER WITHOUT

SHOCK (N=15) FEVER WITH SHOCK (N=23) 60

7 1

2 8

22

GENERAL CONDITION AND ITS SIGNIFICANCE

CONSCIOUS DROWSY

(59)

RESPIRATORY DISTRESS

RESPIRATORY DISTRESS NO OF CASES TOTAL %

PRESENT 33 33%

ABSENT 67 67%

In admissions respiratory distress is seen in 33% of the cases.

PRESENT 33%

ABSENT 67%

RESPIRATORY DISTRESS

(60)

RESPIRATORY DISTRESS OF HFWOS HFWS TOTAL

PRESENT 4 10 19 33

ABSENT 58 5 4 67

SIGNIFICANT

among 100 patients admitted , fever cases with respiratory distress are 33%. In this 33% , 4% of the patients developed only fever,10% patients had hemorrhagic fever without shock.remaining 19%

had hemorrhagic fever with shock with 0.001 pvalue. It shows the significant association of respiratory distress with outcome.

4 10 19

58 5 4

RESPIRATORY DISTRESS AND ITS SIGNIFICANCE

PRESENT ABSENT

(61)

ABDOMINAL DISTENSION

ABDOMINAL DISTENSION NO OF CASES TOTAL %

PRESENT 33 33%

ABSENT 67 67%

In the admissions abdominal distension is seen in 33% of the cases

33%

67%

ABDOMINAL DISTENSION

PRESENT ABSENT

(62)

ABDOMINAL

DISTENSION OF HFWOS HFWS TOTAL

PRESENT 4 10 19 33

ABSENT 58 5 4 67

SIGNIFICANT

among 100 cases , fever cases with abdominal distension are 33%. In this 33% , 4% of the patients developed only fever,10% patients had hemorrhagic fever without shock.remaining 19% had hemorrhagic fever with shock with 0.001 pvalue. It shows the significant association of abdominal distension with outcome.

4 10 19

58

5 4

ABDOMINAL DISTENSION AND ITS SIGNIFICANCE

PRESENT ABSENT

(63)

HEPATOMEGALY

HEPATOMEGALY NO OF CASES TOTAL %

PRESENT 66 66%

ABSENT 34 34%

In admissions hepatomegaly is seen in 66% of the cases clinically.

66%

34%

HEPATOMEGALY

PRESENT ABSENT

(64)

HEPATOMEGALY OF HFWOS HFWS TOTAL

PRESENT 34 12 20 66

ABSENT 28 3 3 34

SIGNIFICANT

among 100 cases admitted , fever cases with hepatomegaly are 66%. In this 66% , 34% of the patients developed only fever,12% patients had hemorrhagic fever without shock.remaining 20% had hemorrhagic fever with shock with 0.009 pvalue. It shows the significant association of hepatomegaly with outcome.

34 12 20

28 3 3

HEPATOMEGALY AND ITS SIGNIFICANCE

PRESENT ABSENT

(65)

DEHYDRATION

DEHYDRATION NO OF CASES TOTAL%

PRESENT 39 39%

ABSENT 61 61%

In the admissions dehydration is seen in 39% of the cases

39

61

DEHYDRATION

PRESENT ABSENT

(66)

DEHYDRATION OF HFWOS HFWS TOTAL

PRESENT 10 9 20 39

ABSENT 52 6 3 61

SIGNIFICANT

OF-ONLY FEVER HFWOS-HEMORRHAGIC FEVER WITHOUT SHOCK HFWS-HEMORRHAGIC FEVER WITH SHOCKT

among 100 cases , fever cases with dehydration are 39%. In this 39% , 10% of the patients developed only fever,9% patients had hemorrhagic fever without shock. remaining 20% had hemorrhagic fever with shock with 0.001 pvalue. It shows the significant association of dehydration with outcome.

10 9 20

52 6 3

DEHYDRATION AND ITS SIGNIFICANCE

PRESENT ABSENT

(67)

WARNING SIGNS

SHOCK NO OF CASES TOTAL %

PRESENT 48 48%

ABSENT 52 52%

In admissions warning signs are seen in 48% of the cases

48%

52%

WARNING SIGNS

PRESENT ABSENT

(68)

WARNING SIGNS OF HFWOS HFWS TOTAL

PRESENT 20 10 18 48

ABSENT 42 5 5 52

SIGNIFICANT

among 100 cases admitted , fever cases with warning signs are 48%. In this 48% , 20% of the patients developed only fever,10% patients had hemorrhagic fever without shock. remaining 18% had hemorrhagic fever with shock with 0.001 pvalue. It shows the significant association of warning signs with outcome.

2 1 17

60 14 6

WARNING SIGNS AND ITS SIGNIFICANCE

PRESENT ABSENT

(69)

TOTAL COUNT

TOTAL COUNT NO OF CASES TOTAL %

LEUKOPENIA 52 52%

NORMAL 33 33%

LEUCOCYTOSIS 15 15%

In admissions leukopenia is seen in 52% of the cases. leucocytosis is seen in 15%

LEUKOPENIA 52%

NORMAL 33%

LEUCOCYTOSIS 15%

TOTAL COUNT

(70)

TOTAL COUNT OF HFWOS HFWS TOTAL

LEUKOPENIA 33 7 12 55

NORMAL 27 4 2 33

LEUCOCYTOSIS 2 4 9 12

SIGNIFICANT

33

7

12 27

4 2

2 4

9

0 5 10 15 20 25 30 35

TOTAL COUNT AND ITS SIGNIFICANCE

LEUKOPENIA NORMAL LEUCOCYTOSIS

(71)

PLATELET COUNT

PLATELET COUNT NO OF CASES TOTAL %

< 1 LAKH 49 49%

> 1 LAKH 51 51%

In admissions platelet count is less than 1 lakh in 49% of the patients

51% 49%

PLATELET COUNT

< 1 LAKH

> 1 LAKH

(72)

PLATELET COUNT OF HFWOS HFWS TOTAL

< 1 LAKH 18 12 19 49

> 1 LAKH 44 3 4 51

SIGNIFICANT

among 100 cases admitted , fever cases with less than 1 lakh are 49%. In this 49% , 18% of the patients developed only fever,12% patients had hemorrhagic fever without shock. remaining 19% had hemorrhagic fever with shock with 0.001 pvalue. It shows the significant association of platlet count with outcome.

18 12 19

44 3 4

PLATELET COUNT AND ITS SIGNIFICANCE

< 1 LAKH > 1 LAKH

(73)

PACKED CELL VOLUME

PCV NO OF CASES TOTAL %

< 40 61 61%

> 40 39 39%

In admissions packed cell volume more than 40 is seen in 61% of the cases.

61%

39%

PCV

< 40

> 40