In Gilgit she was being treated for genitourinary tuberculosis without any documentary evidence and was started on emirical ATT

The symptoms for which she was being treated was dysurea, fever and weight loss

? She had high grade fever for the last 4-6 months, intermittent no associated chills/rigors, she had dysurea initially but at present there was no such complaints, no cough, rashes, joint pains, unusual hair loss but she had mod. To severe Rt. Upper abdomen and epigastric pain for the last 1 month which was constant was non radiating associated with 4-5 episodes of vomitings per day which contains around ? cup of fresh blood witheach episode and positive H/O malena. Few days prior to admission she was transfused with 5 PRBC in gilgit

? She was found jaundiced by her physician in gilgit one month back and the ATT was stopped she took ATT for two months without any subjective or objective improvement, rather she was deteriorated during that period.

? There was no significant past medical or surgical history of note.

? She was a mother of 8 children all are alive and healthy, her husband is also alive and had no medical/surgical problem.

EXAM:

On physical exam she was middle aged lady with toxic look lying on the bed, pale and jaundiced with B/L pitting pedal edema extending up to the knees, there was no lymphadenopathy, asterexis, joint tenderness

Vitals:

B.P 100/50 pulse 110/min regular

She was febrile with the temp of 38.6 C

R/R was 22/min Spo2 96% on room air

Respiratory Exam:

She was tacyponic with the R/R of 22/min but not using her accessory muscles of breathing, trachea was central, apex beat was not displaced, fine basal crepts were present posteriorly on auscultation

CVS Exam:

Apex beat was palpable in 5 ICS, normal in character, s1 and s2 of normal intensity were audible in all four areas with no added sounds

CNS:

She was alert and orientedx3, no gross cranial, sensory or motor deficit, pupils BERL and both plantars were normal

Abdomen:

Distended with flat umlicus and white stria, severe Rt hypochondrial tenderness even on superficial palpation liver seems to be enlarged but due to tenderness it was difficult to comment,there was no splenomegaly but positive shifting dullness and normal audible gut sounds.

? She was empirically started on broad spectrum antibiotics, IV fluids, NG was passed and opiod analgesic on PRN basis and kept NPO, DRE was pos for malena, in the mean while gastro service was involved

? He was treated in ER with valium, valproate, phenytoin, ceftriaxone, magnesium, calpol suppositories and, IV NS with KCL @ 4 meq/hr.

? EEG done in ER showing mild diffuse slowing

? He arrived at 1915 HRS in SCU and after the above examination finding so our first impression was encephalitis/metabolic encephalopathy/cyclosporin toxicity.

? His ECG was normal.

? CXR showed pneumonic consolidation in the left mid lung zone.

? CT Head without contrast (20/2/06) showed left frontal lobe infarct

? CSF DR (20/2/06): Glu 49, prot 156.1, TLC 200, Polys 70, Lym 30, RBC 13800

? Echo was done which was normal there was no vegetation seen.

? Gastro service was also involved regarding chronic liver disease they agreed with the same treatment.

? In SCU he was treated with meropenam and acyclovir in renally adjusted dose, IV fluid and potassium and magnesium replacement, phenytoin and vancomycin (stat dose).

ID-20/2/06 (Dr. Bushra Jamil) sugggested HSV PCR, CMV PCR (which was already sent), MRI head with contrast, sputum C/S, AFB, fungal smear, she agreed with the rest of the treatment.

During her stay in hospital he was dialysed thrice (22, 23 and 27, feb 2006) in view of decreased urine output and uremia

? MP ICT 20/2/06: -ve

? UDR: leuco 20, RBC 10, Nitrite ?ve, Hb +1, Protein +1.

? AntiHCV Ab (20/2) reactive

? HBsAg (20/2) reactive

? Cyclosporin level: 62.6 mg/ml (20/2)

? Serum valproate and phenytoin levels were with in therapeutic range.

? CSF DR (23/2): gluc 40, prot 151.6, TLC 100, poly 55, lymp 45, RBC 900.

? US ABD (20/2) minimally coarse echotexture of liver, dilated portal vein with minimal peripancreatic varices seen, mild ascites, only transplanted kidney visualised in the RIF.

? Neurology service (Dr.Mughis) was involved (21/2/06) and he did not agree with the CT head report with the radiologist, his opinion was abscess not an infarct. CT head with contrast was done as advised by neurology which did not showed any contrast enhancement of the left frontal lesion so this most likely represent an infarct.

? Dr. Mughis asked for the second opinion from Dr. Wasay and both the neurologist agreed on MRI head and suggested repeat CSF DR. which was done (gluc 40, protein 151.6, TLC 100, poly 55, lymphos 45, RBC 900) MRI brain was done which showed multiple ring enhancing leisions in the frontal lobe.

? On 21 Feb Dr. Bushra Jamil reviewed the patient and she suggested to add IV Ganciclovir and Amphotericin along with Meropenam and Vancomycin along with paranasal sinus endoscopy (suspecting inflammation of right ethmoid sinus on CT Head) and biopsy.

? ENT opinion was sought on the same day and Dr. Mughira did rigid endoscopy of the nose for suspecting fungal sinusitis (mucormycosis), washings and biopsy from left middle meatus was done and fugal smear and CS was sent which turned out to be negative afterwards

EEG was repeated for generalised jerking as advised by neurology service on 22/2/2006 which showed diffuse theta slowing.

? Pumonology service was also invoved in view of non resolving pneumonia.

? Dr. Javed Khan had seen the pt. and advised bedside bronchoscopy which was done on 24 feb. bronchial washing sent for gram stain, CS, AFB smear and AFB CS, fungal smear and CS which later turned out to be negative.

? On 24 feb 2006 ID review suggested to discontinue ganciclovir and send toxoplasma titres, CMV serology (already sent), empiric ATT considering his immunocompromised status and persistent fever of 38o C and neck rigidity (which was the new development).

? ID review also suggested brain lesion biopsy.

? Neurosurgery consult was generated on the same day and they planned burr hole biopsy of the brain lesion after discussing all the possible consequences with the family on 27 feb 2006.

? But the patient condition was deteriorating and he was having bradycardia and hypertension which might be because of raised intracranial pressure.

? He was treated with mannitol, steroids were already on the board.

? Neurosurgery (Dr. Khalid Chishti) suggested to postpone the brain biopsy as the patient was not hemodynamically stable.

? ID follow up by Dr. Maqsood Bhatti done on March 1, 2006 and ATT (4 drugs Regime) and Septran DS (to cover PCP/Toxoplasmosis) was started as advised by ID attending.

? On March 2, 2006 his condition was furthur deteriorated and his BP started to fall, all his antihypertensives were stopped and prognosis and outcome rediscussed with the family they ageed to keep the patient no code and they were planning to take him to home.

? On the same day patient was shifted under care of Dr. Mehmood Riaz, code rediscussed with the family and code status remained unchanged (no code, no ionotropic support) but the patient condition was the same and perhaps deteriorated furthur (GCS=3/15).

? On the same day, March 3, 2006, 1543 hrs our team and his family members faced the demise of this young soldier.

?TIMING AND ETIOLOGY OF POSTTRANSPLANT INFECTION

? <1 month posttransplant:

? Nosocomial pneumonia, wound infection, UTI, catheter related sepsis.

?ETIOLOGY: Bacterial or fungal infections.

? 1-6 mo posttransplant:

? Opportunistic infections.

?ETIOLOGY: CMV, PCP, Aspergillus spp., toxoplasma gondii, listeria monocytogenes, varicella-zoster virus

? Reactivation of preexisting infections

?ETIOLOGY: Mycobacteria spp. Endemic mycosis.

? >6 mo posttransplant:

? Community-acquired infections

?ETIOLOGY: Bacterial

? Chronic progressive infections

?ETIOLOGY: HBV, HCV, CMV,EBV, Papillomavirus, polyoma virus (BK)

? Opportunistic infections

?ETIOLOGY: PCP, L. monocytogenes, Nocardia asteroides, Crytococcus neoformans, Aspergillus spp.