An Intresting Case of Fever with Rash
Transcription
An Intresting Case of Fever with Rash
DR. CHAITANYA H. BALAKRISHNAN GUIDES: DR. H.V. NATARAJU, PROFESSOR AND H.O.D., DR. YOGITHA C. DR. PRADEEP C. DEPT. OF GENERAL MEDICINE, KIMS HOSPITAL A 27 year old male, Mr. J, came with the following: CHIEF COMPLAINTS: Fever Since 10 Days Joint swelling Since 7 Days Rashes Since 6 Days Facial Puffiness Since 2 Days HISTORY OF PRESENTING ILLNESS: Fever- intermittent type, associated with chills Joint swelling- large and small joints, associated with severe joint pain, progressive Rashes- started over the hands and feet, then spread to involve the arms, legs, chest, back and abdomen, reddish lesions, not associated with itching Facial puffiness- more in the morning, decreases as the day passes, not a/w decreased urine output No h/o bleeding manifestations, cough, breathlessness, throat pain No h/o chest pain, abdominal pain, urinary/ bowel disturbances No h/o headache, vomiting, giddiness PAST HISTORY: no h/o similar complaints in the past, no other co-morbidities FAMILY HISTORY: nothing significant PERSONAL HISTORY: nothing significant PULSE: 126/min BLOOD PRESSURE: 140/86mm hg RESPIRATORY RATE: 22/min Edema present- bilateral lower limb edema upto ankles, pitting Facial puffiness present No pallor, icterus, clubbing, lymphadenopathy, cyanosis. SKIN AND MUCOSA: maculopapular rash present over upper limbs, chest, back and abdomen –blanchable palpable purpura present over bilateral lower limbs petechiae over the soft palate JOINTS: swelling of ankle joints bilaterally, proximal and distal interphalangeal joints of both hands PURPURA OVER WRIST, FOREARM AND PALMS PETECHIAE OVER BACK PALPABLE PURPURA OVER LOWER LIMBS INCLUDING DORSUM OF FEET RESPIRATORY SYSTEM: No abnormality detected CARDIOVASCULAR SYSTEM: Tachycardia present, no murmurs ABDOMEN EXAMINATION: Hepatomegaly present 2cm below the R.C.M.( soft, rounded borders, non tender), bowel sounds heard CENTRAL NERVOUS SYSTEM: No abnormality detected VIRAL EXANTHEMATOUS FEVER WITH ARTHRITIS- ? ARBOVIRAL DISEASE RICKETSIAL FEVER VASCULITIS DAY 1: Hb: 14.7g% TC: 21790 cells/mm3 DC: P82.9, L12, M4.3 ESR: 36mm/hr Platelet count: 1.37 lakh/mm3 B. Urea: 28mg/dl S. Creatinine: 1.3 mg/dl Urine routine: alb++, sug nil, PC 15-20cells/hpf, RBCplenty ECG: sinus tachycardia CXR: normal DAY 1: QBC FOR MP: Positive for plasmodium vivax Peripheral smear: normocytic normochromic blood picture with neurophilic leukocytosis and no evidence of malarial parasites Sepsis work up: positive( CRP, S. Procalcitonin, FDP) Widal test,HIV, HbsAg, VDRL, Weil Felix test: Negative DAY 1: USG Abdomen and pelvis: Borderline splenomegaly, Grade 1 Medical Renal Disease Blood C/S- no growth, Urine C/S- Enterococcus PT with INR- normal LFT: TB DB OT PT ALB GLO ALKP 0.5 0.2 76 105 2.9 6.7 164 SEPSIS- ? UROSEPSIS COMPLICATED PLASMODIUM VIVAX INFECTION RICKETSIAL FEVER VASCULITIS Patient was started on broad spectrum antibiotics( piperacillin-tazobactum), artesunate and primaquine, antipyretics, doxycycline, antiinflammatory drugs and IV fluids. By day 3, patient was symptomatically better: reduction in the joint pains and swelling blanchable rash over the trunk and chest was fading Purpura remained persistent over both lower limbs DAY 3: TC: 15710/mm3 DC: N79, L11, M5, E3 Platelet count: 1.48 lakh/mm3 S. Creatinine 1.2mg/dl S. Calcium 9.2 mg/dl S. Phophate 2.8mg/dl S. Albumin 2.2mg/dl Urine routine: alb ++, PC 13-15/hpf, RBC 25-30/hpf By day 5, patient was afebrile with complete reduction in the joint swelling and disappearance of the chest and abdominal rash but purpura remained persistent. Patient was continued on IV antibiotics as per the urine C/S report. DAY 5: TC: 9900/mm3 Platelet: 1.61 lakh/mm3 S. Creatinine: 1.0 mg/dl Urine spot protein-creatinine ratio: 1.45(normal <1) 24 hour urinary protein: 1750mg/dl(nephritic range) Skin biopsy of palpable purpura: leukocytoclastic vasculitis NEUTROPHILIC INFILTRATES WITH FIBRIN DEPOSITS ? HENOCH SCHONLEIN PURPURA SECONDARY TO ENTEROOCCUS INFECTION CO-INFECTED WITH PLASMODIUM VIVAX MALARIA Patient was discharged after 1 week of hospital stay and was to review with repeat urine routine, 24 hour urinary protein after 1 week. After 1 week, urine routine showed persistent albuminuria and hematuria with a 24 hour urinary protein of 2265mg/dl. Hence the patient was re-admitted for a renal biopsy. Renal biopsy: Glomeruli- Segmental mesangial cell proliferation with endocapillary proliferation with 25% crescent formation Tubules- RBC’s in the lumen but no atrophy Vessels- mild hyperplasia with intimal hyalinosis Immunofluroscence- diffuse global fine granular deposits of IgA and C3, few IgG and IgM FINAL DIAGNOSIS: Henoch Schonlein Purpura with ISRDC classification IIIa without chronicity AFFECTED GLOMERULUS MESANGIAL PROLIFERATION PAS NEGATIVE NORMAL TUBULES WITH MESANGIAL PROLIFERATION International Study Group of Kidney Disease in Childhood, uses crescents as a critical factor. In this schema, grade I has minimal alterations, grade II is pure mesangial proliferation, and grades III to V have focal segmental or diffuse proliferation with <50%, 50 to 75%, or >75% crescent formation, respectively. Grade VI has glomeruli with a membranoproliferative pattern of injury, found in 2% of biopsies. The patient was started on steroid pulse therapy for 5 days(IV Methylprednisolone 500mg OD) and discharged on oral prednisone for 6 weeks. Patient is a regular at the follow up OPD and latest urine routine revealing traces of albumin with RBC’s 3-5. HENOCH SCHONLEIN PURPURA SECONDARY TO ENTEROCOCCUS INFECTION WITH PLASMODIUM VIVAX CO-INFECTION Henoch-Schönlein purpura (HSP; also referred to as Schönlein-Henoch purpura, anaphylactoid purpura, or purpura rheumatica) is an acute immunoglobulin A (IgA)–mediated disorder characterized by a generalized vasculitis involving the small vessels of the skin, the gastrointestinal (GI) tract, the kidneys, the joints, and, rarely, the lungs and the central nervous system (CNS). It is a subset of necrotizing vasculitis characterized by fibrinoid destruction of blood vessels and leukocytoclasis. The prevalence of HSP peaks in children aged 3-10 years, but the condition is also seen in adults. The dominant clinical features of HSP include: cutaneous purpura Arthritis abdominal pain, GI bleeding, orchitis nephritis. In one half to two thirds of children, an upper respiratory tract infection (URTI) precedes the clinical onset of HSP by 1-3 weeks. The most serious complication of HSP is renal involvement, which occurs in 50% of older children but is serious in only approximately 10% of patients. In 80% of patients, renal involvement becomes apparent within the first 4 weeks of illness. Overall, 2-5% of patients progress to end-stage renal failure (ESRD). The renal biopsy features include acute glomerular lesions like mesangial hypercellularity, endocapillary proliferation, necrosis, cellular crescents, and leukocyte infiltration. Allergens, such as foods, horse serum, insect bites, exposure to cold, and drugs (eg: ampicillin, erythromycin, penicillin, quinidine, and quinine), may precipitate the illness. Infectious causes include: Bacteria (eg, Group A streptococcus, Haemophilus parainfluenzae, Campylobacter Mycoplasma, Legionella, Yersinia, Shigella, or Salmonella) Viruses (eg, adenoviruses,Epstein-Barr virus [EBV], parvoviruses, or varicella-zoster virus [VZV]). Vaccines such as those against cholera, measles, paratyphoid A and B, typhoid, and yellow fever have also been implicated. TREATMENT: Management of HSP includes adequate hydration; immediate discontinuance of any exposure to antigenic stimulants and follow-up each week for the first month, every other week for the second month, and monthly thereafter until abnormal urinary findings subside. Nephropathy is treated supportively. Patients’ fluid and electrolyte balance should be monitored, their salt intake should be restricted, and antihypertensives should be prescribed when needed. TREATMENT: Methyl Prednisolone 1g/ day for 3 days(pulse therapy) followed by prednisone in a dosage of 1 mg/kg/day for 2-4 weeks and then tapered over 2 more weeks is used in HSP nephropathy. Other treatment regimens have included IV or oral steroids with or without any of the following: ▪ Azathioprine ▪ Cyclophosphamide ▪ Cyclosporine ▪ Dipyridamole ▪ High-dose IV immunoglobulin G (IVIg) ▪ Danazol HSP is a disease that may affect the adult population precipitated by viral/bacterial infections or even allergens and drugs presenting with rash, fever, abdominal and renal involvement. The disease is self limiting and the treatment is conservative with steroids or plasmapheresis only in rapidly progressing renal disease. “Henoch-Schönlein Purpura Nephritis”; Anup Rai, Cynthia Nast And Sharon Adler; JASN 1999 “Henoch-Schönlein Purpura Nephritis”: Pathophysiology, Treatment, and Future Strategy; Jean-Claude Davin; CJASN 2001. “Henoch-SchöNlein Purpura in Adults:; María José López Meiller, Javier Alberto Cavallasca, María del Rosario Maliandi, and Gustavo Guillermo Nasswetter- PubMed Clinics 2007.