CASE PRESENTATION

By:Dr. ZULAIKHA MALIKPGR WMW

BIODATA

NAME: SHAHID

AGE: 33yrs

SEX: male

MARITAL STATUS: single

RESIDENT OF: KAREEM PARK,lahore

OCCUPATION: tailor

D.O.A. : 25/10/14

M.O.A. : ER

PRESENTING COMPLAINTS

FEVER 7 DAYS

VOMITING 3 DAYS

OLIGURIA 2 DAYS

YELLOW DISCOLRATION OF SCLERA 2 DAYS

HOPIMy patient was in his usoh 7 days back when he started having fever that was acute,continuous,high grade,with rigors and chills,relieved temporarily by medication .

There is no h/o cough/sputum, burning micturition,diarrhoea,joint pains,jaundice,SOB.

Patient had c/o vomiting for 3 days which was acute,non bilious,projectile,contained food particles and started even with a sip of water.

Pt c/o decreased urine for the last 2 days

Pt c/o yellow discolration of sclera for 2 days

HOPI contd: There is no h/o cough,sputum,hemoptysis or wheeze or allergies.no h/o tb contact

No h/o orthopnea,PND,pedal edema.palpitations, chest pain.

There is no h/o dizzines,blackouts,headache,tingling, numbness or weakness of any side of the body No history of chest pain, palpitations, syncope, orthopnea, PND or pedal edema..

No history of abdominal pain, diarrhea, constipation, vomitting,urinary frequency,urgency,burning micturation or any genital ulcers..

No history of difficulty standing from sitting posture

HISTORY CONTINUED..

PAST HISTORY: no history of hospital admission for any complaint

SURGICAL HISTORY: insignificant

DRUG HISTORY: pt was a non smoker non addict .h/o iv drug abuse was negative.

NO H/O EXPOSURE TO RAT S

PERSONAL HISTORY:non diabetic,nonhypertensive,non-smoker.no h/o IHD

FAMILY HISTORY:insignificant .

SOCIO-ECONOMIC: belongs to middle class..

1.ACUTE PANCREATITIS

2.ACUTE GASTRITIS

3.ACUTE HEPATITIS

4.LEPTOSPIROSIS

5.AKI DUE TO UROSEPSIS

EXAMINATION

A young male of average height and built,lying in bed, with branula over His right hand having following vitals:

PULSE: 110/min

B.P. : 170/90 mmHg

TEMP: Afebrile

R/R: 16/min

GPE: PALLOR ++

Jaundice +

PEDAL EDEMA+

FACIALPUFFINESS +

GENERALIZED BODY SWELLING +

RIGHT PAROTID SWELLING +

CYANOSIS –

JVP.NOT RAISED

LYMPHADENOPATHY –

SYSTEMIC REVIEWGIT

inspection

abdomen scaphoid, normal pattern of hair distribution,no striae, scar mark or visible pulsations,normal pattern of breathing,hernial orifices intact.no bruises or discoloration around umbilicus (cullen’s sign negative).no bruises in flanks (grey turner sign negative)

PALPATION:

Superficial palpation: unremarkable

DEEP PALPATION:

abdomen is tender all over especially in the epig region.

no mass palpable

no visceromegaly

b/s audible(2sets/min)

PERCUSSION:

FLUID THRILL –

FLANK DULLNESS –

AUSCULTATION:

BS ++

CNS :

GCS 11/15..

HMF,CN:intact

SOMI –

PUPILS B/L REACTIVE

PLANTARS B/L MUTE

SENSORY SYSTEM: couldn’t be assessed PROPERLY BUT WITHDRAWS ON PAINFUL STIMULUS

MOTOR:normal bulk,tone,power and reflexes,bothupper limbs and lower limbs

FUNDOSCOPY:normal

CVS :

INSPECTION:No visible pulsations,striae or scar mark

APEX BEAT:in 5th ICS,midclavicular line.

S1+S2:of normal intensity and character with no added sound

No pericardial rub

RESP:

No chest deformity with thoraco-abdominal breathing pattern

Trachea central

Chest expansion:4cm

Normal vocal fremitus bilaterally

Auscultation:NVB with bilateral equal air entry .no added sounds,normal vocal resonance,no pleural rub..

CASE SUMMARY

a young male with h/o continuous high grade fever with rigors and chills for 7 days and projectile vomiting for 7 days with no h/o asoc.and jaundice for 2 days.

on examination he is drowsy but responsive,has tachycardia,hypertension, tender abdomen,b/l pitting pedal edema,oliguria but no dysuria or hematuria or pain in flanks

ACUTE PANCREATITIS

AKI DUE TO UTI

LEPTOSPIROSIS

ACUTE HEPATITIS

PROGRESS25/10At admission

26/10

27/10AFTER 48 HRS

28/10

29/10 30/10 31/10

HB 14

TLC 34 12.5

UREA 88 92

CREAT 6 7 9 11 11.9 13

AMYLASE 273 161 352

LIPASE 103 323 218

LDH 370 808 1103

CA 7 7 7.2

ALT/AST 158/294 746/276

450/85

26/10 28/10 30/10

ABG’S PH 7.34PO2PCO2 27HCO3 1502 SAT 92%

PH 7.36PO2PCO2 27HCO3 16O2 SAT

CKMB/CKNAC 266/110 60/125

NA/K 132/4.2 135/5.8 133/5.3

PT/APTT 19/33

TGHDLCHOL

45232 185

BILDIRECT BILINDIRECT BIL

1.1 95.93.2

LABS

HEP CHEP BHIV BY KIT

HIV BY ELISA

URINE COMPLETE

NEGATIVENEGATIVEWEAKLY POSITIVENEGATIVE

PUS CELLS 8-10BLOOD -GLUCOSE -KETONES NILPROTEIN +2

FURTHER PLAN :

LEPTOSPIRAL ANTIBODIES WERE AWAITED

Ct brain plain

Ct contrast abdomen

Mri abdomen

Gamma GT

CXR: NORMAL

USG Abd: fatty liver

ECG: SINUS TACHYCARDIA

CXR:

NOT AVAILABLE

ECG

FINAL DIAGNOSIS

ACUTE PANCREATITIS

TREATMENT GIVEN IN WARD

INJ MERONEM 5OOMG IV BD

INJ FLAGYL 500MG IV TDS

INJ ISOKET @ 30 DPM

INJ RISEK 40MG IV BD

INJ LASIX 60MG IV BD

INJ CA GLUCONATE IV TDS

INF N/S 1000CC IV OD

INF 5% D/W 1000ML +1AMP HEPAMERZ IV BD

INJ METOMIDE IV TDS

INJ TRANSAMINE 250MG IV TDS

INJ AMINOVIL 500ML IV OD

INJ TANZO 2.25G IV TDS

INJ OXIDIL 1G IV BD

TAB MINIPRESS 1MG PO TDS

TAB NORVASC 10MG PO OD

STAT ORDERS

INJ SOLUCORTEF 250MG STAT

INJ HYDRALAZINE20MG IV IN 100ML N/S OVER 15 MIN

INJ AMINOVIL 500MG IV OD

DUPHALAC ENEMA STAT

INJ OXIDIL 1D IV BD

TREATMENT IN THE HDU:

TREATMENT OF UNCONTROLLED HYPERTENSION

IOP MONITORING

ANTIBIOTIC PROPHYLAXIS

TERMINAL EVENTS:

PT DETERIORATED BY DAY 5 .DEC IN URINE OUTPUT.PLAN FOR HD WAS MADE.PT WENT FOR IST SESSION OF HD BUT COULD NOT MAKE IT.PT HAD UNCONTROLLED HYPERTENSION.PT COLLAPSED AT THE START OF THE DIALYSIS SESSION AND BSL WAS 48.HE WAS BPLESS AND PULSELESS.HE WAS IMMEDIATELY SENT TO EMERGENCY ICU .CPR WAS DONE AND PT WAS RESUSCITATED BUT OF NO AVAIL.

COMPLICATIONS OF DIALYSIS:

Hypotension

A decrease in blood pressure is the most frequent complication reported during hemodialysis. When fluid is removed during hemodialysis, the osmotic pressure is increased and this prompts refilling from the interstitial space. The interstitial space is then refilled by fluid from the intracellular space. Excessive ultrafiltration with inadequate vascular refilling plays a major role in dialysis induced hypotension. The immediate treatment to hypotension is to discontinue dialysis and place the patient in a trendelenburg position. This will increase cardiac filling and may increase the blood pressure promptly.

Cramps

In the majority of hemodialysis patients, cramps occur toward the end of the dialysis procedure after a significant volume of fluid has been removed by ultrafiltration. The immediate treatment for cramps is directed at restoring intravascular volume through the use of small boluses of isotonic saline. Prevention of cramps has been attempted with the prophylactic use of quinine sulfate at least 2 hours prior to dialysis.

Arrhythmia

Patients on maintenance hemodialysis are at risk of cardiac arrhythmias. They occur predominately in association with hemodialysis or may occur in the interdialytic period. Both acute and chronic alterations in fluid, electrolyte, and acid-base homeostasis may be arrhythmogenic in these patients.

Hemolysis

Hemolysis may result from a number of biochemical and toxic insults during the dialysis procedure. The half-life of red blood cells in renal failure patients is approximately one half to one third of normal and the cells are particularly susceptible to membrane injury.

Febrile reactionsFebrile episodes should be aggressively evaluated with appropriate wound and blood cultures. The suspicion of infection should be high. Treatment of endotoxin related fever is generally supportive with antipyretics. Temperatures should be recorded at the initiation and termination of dialysis treatment.

HypoxemiaA fall in arterial PO2 is a frequent complication of hemodialysis that occurs in nearly 90% of patients. The drop ranges from 5 to 35 mm Hg, and reaches its peak between 30 - 60 minutes after beginning dialysis. This is obviously undesirable for patients with underlying cardiopulmonary disease. Also, patients on mechanical ventilators with constant minute volume and inspired oxygen concentration can still develop hypoxemia during hemodialysis.

ACUTE

PANCREATITIS

ACUTE PANC

Acute pancreatitis or acute pancreatic necrosis[1] is a sudden inflammation of the pancreas. It can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures, such as NPO (nil per os, fasting) and aggressive intravenous fluid rehydration, severe cases may require admission to the intensive care unit or even surgery to deal with complications of the disease proces

S/S

The most common symptoms and signs include:

severe epigastric pain (upper abdominal pain) radiating to the back,severe,boring,gets worse on lying supine and walking.

nausea

vomiting

loss of appetite

Fever

chills (shivering)

hemodynamic instability, which include shock

tachycardia (rapid heartbeat)

respiratory distress

peritonitis

LESS COMMON SIGNS

Signs which are less common, and indicate severe disease, include:

Grey-Turner's sign (hemorrhagic discoloration of the flanks)

Cullen's sign (hemorrhagic discoloration of the umbilicus)

Pleural effusions (fluid in the bases of the pleural cavity)

Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to local toxic lesion of the vessels)

Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6–7 cm above the umbilicus))

Kamenchik's sign (pain with pressure under the xiphoid process)

Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA))[2]

CAUSES Most common causes

Alcohol

Gallstones

Metabolic disorders: hereditary pancreatitis, hypercalcemia, hyperlipidemia, malnutrition

ERCP

Abdominal trauma

Penetrating ulcers

Carcinoma of the head of pancreas, and other cancer

Drugs: diuretics (e.g., thiazides, furosemide), gliptins e.g., vildagliptin, sitagliptin, saxagliptin, linagliptin, tetracycline, sulfonamides, estrogens, azathioprine and mercaptopurine, pentamidine, salicylates, steroids[citation needed]

Infections: mumps, viral hepatitis, coxsackievirus, cytomegalovirus, Mycoplasma pneumoniae, Ascaris

Structural abnormalities: choledochocele, pancreas divisum

Radiation X-ray

Assessment of severity:

RANSON CRITERIA

SOFA SCORE

APACHE 2 SCORE

BISAP SCORE:

Used to assess the sverity in the first 24 hrs at the bedside.IT IS USED TO IDENTIFY PTS AT RISK OF MORTALITY

BUN> 25(THE RATE OF INC IN BUN IS PROPORTIONATE TO THE RISK FOR MORTALITY)

impaired mental status

SIRS

AGE>60

PLEURAL EFFUSION

PATHOGENESIS

In mild pancreatitis

there is inflammation and edema of the pancreas.

In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of zymogens and inappropriate activation of pancreatic zymogens inside the pancreas, most notably trypsinogen. Normally, trypsinogen is activated to trypsin in the duodenum where it assists in the digestion of proteins. During an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically cathepsin, with trypsinogen. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death according to either the necrosis or apoptosis mechanism (or a mix between the two). The balance between these two processes is mediated by caspases which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate.

As part of the initial injury there is an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage

DIAGNOSIS

Acute pancreatitis is diagnosed clinically but requires CT evaluation to differentiate mild acute pancreatitis from severe necrotic pancreatitis. Experienced clinicians were able to detect severe pancreatitis in approximately 34-39% of patients who later had imaging confirmed severe necrotic pancreatitis. Blood studies are used to identify organ failure, offer prognostic information, determine if fluid resuscitation is adequate, and if antibiotics are indicated.

]

BLOOD INVESTIGATIONS

Full blood count,Renal function tests,

Liver Function,serum calcium,

serum amylase and lipase,Arterial blood gas, Trypsin-Selective Test[7

GOLD STANDARD INVESTIGATION

Imaging - A triple phase abdominal CT and abdominal ultrasound are together considered the gold standard for the evaluation of acute pancreatitis. Other modalities including the abdominal xray lack sensitivity and are not recommended. An important caveat is that imaging during the first 12 hours may be falsely reassuring as the inflammatory and necrotic process usually requires 48 hours to fully manifest.

Labs

Elevated serum amylase and lipase levels, in combination with severe abdominal pain, often trigger the initial diagnosis of acute pancreatitis. However, they have no role in assessing disease severity.

Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment.

Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia.

Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase), bowel obstruction, infarction, cholecystitis, and a perforated ulcer.

If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to alcohol.[8]

Decreased serum calcium Glycosuria

COMPUTED TOMOGRAPHY

CT is an important common initial assessment tool for acute pancreatitis. Imaging is indicated during the initial presentation if:

the diagnosis of acute pancreatitis is uncertain

there is abdominal distension and tenderness, fever>102, or leukocytosis

there is a Ranson score > 3 or APACHE score > 8

there is no improvement after 72 hours of conservative medical therapy

there has been an acute change in status: fever, pain, or shock

MRI:

While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis,[14] magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris.[15]

Additional utility of MRI includes its indication for imaging of patients with an allergy to CT's contrast material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms, and venous thrombosis.[16]

RANSON SCORE

Ranson criteria is a clinical prediction rule for predicting the severity of acute pancreatitis. It was introduced in 1974.[1]

At admission age in years > 55 years

white blood cell count > 16000 cells/mm3

blood glucose > 10 mmol/L (> 200 mg/dL)

serum AST > 250 IU/L

serum LDH > 350 IU/L

At 48 hours:

serum calcium < 8.0 mg/dL)

Hematocrit fall >10%

ARTERIAL PO2 < 60 mmHg)

BUN RISE BY 5 or more mg/dL

Base deficit (negative base excess) > 4 mEq/L

Sequestration of fluids > 6 L

MORTALITY PREDICTION :

SCORE % MORTALITY

0-2 1%

3-4 16%

5-6 40%

7-8 100%

APACHE SCORE

"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 8 points predicts 11% to 18% mortality

Hemorrhagic peritoneal fluid

Obesity

Indicators of organ failure

Hypotension (SBP <90 mmHG) or

tachycardia > 130 beat/min

PO2 <60 mmHg

Oliguria (<50 mL/h) or increasing BUN and creatinine

Serum calcium < 1.90 mmol/L (<8.0 mg/dL)

serum albumin <33 g/L (<3.2.g/dL)

GLASGOW CRITERIA The Glasgow criteria is valid for both gallstone and alcohol induced

pancreatitis, whereas the Ranson score is only for alcohol induced pancreatitis. If a patient scores 3 or more it indicates severe pancreatitis and the patient should be transferred to ITU. It is scored through the mnemonic, PANCREAS:

P - PaO2 <8kPa

A - Age >55 year old

N - Neutrophilia - WCC >15x10(9)/L

C - Calcium <2 mmol/L

R - Renal function, Urea >16 mmol/L

E - Enzymes: LDH >600iu/L; AST >200iu/L

A - Albumin <32g/L (serum)

S - Sugar: blood glucose >10 mmol/L

TREATMENT OF MILD DISEASE

NPO

PAIN CONTROL BY MEPRIDINE 100-150MG I/M EVERY 4 HRS

RESUME ORAL FLUIDS ONLY WHEN PAIN IS SETTLED,BOWEL SOUNDS ARE AUDIBLE.

CLEAR LIQUIDS ARE GIVEN FIRST

SHIFT TO FAT FREE DIET LATER

TREATMENT OF SEVERE DISEASE:

500-1000ML FOR SEVERAL HRS THEN 250-3—ML TO MAIINTAIN INTRAVASCULAR VOLUME.

MONITOR CA LEVELS AND REPLACE ACCORDINGLY

ALBUMIN OR FFP INFUSIONS FOR PATIENT WITH COAGULOPATHY OR HYPOALBUMINEMIA

MONIOTR ABGS N CVP FOR FLUID REPLACEMENT

ANTIBIOTIC PROPHYLAXIS

FLUID REPLACEMENT

Aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (eg, normal saline or lactated Ringer’s solution) to all patients with acute pancreatitis, unless cardiovascular, renal, or other related comorbid factors preclude aggressive fluid replacement.

In patients with severe volume depletion that manifests as hypotension and tachycardia, more rapid repletion with 20 mL/kg of intravenous fluid given over 30 minutes followed by 3 mL/kg/hour for 8 to 12 hours.[30][31]

Fluid requirements should be reassessed at frequent intervals in the first six hours of admission and for the next 24 to 48 hours. The rate of fluid resuscitation should be adjusted based on clinical assessment, hematocrit and blood urea nitrogen (BUN) values.

35]

There is some evidence that fluid resuscitation with lactated Ringer’s solution may reduce the incidence of Systemic Inflammatory Response Syndrome (SIRS) as compared with normal saline.[36]

PAIN CONTROL

Meperidine, has been favored over morphinefor analgesia in pancreatitis because studies showed that morphine caused an increase in sphincter of Oddi pressure

BOWEL REST

In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving him or her nothing by mouth, giving intravenousfluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest.

Approximately 75% of relapses occur within 48 hours of oral refeeding.

NUTRITIONAL SUPPORT

Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as fungemia).

Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the trachea even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea). Oxygen may be provided in some patients (about 30%) if Pao2 levels fall below 70mm of Hg.

ANTIBIOTICS(Carbapenems)

IMIPENEM:

0.5 gram intravenously every eight hours for two weeks showed a reduction in from pancreatic sepsis from 30% to 12%.

CEFUROXIME 1.5 G IV TDS FOR 14 DAYS REDUCES THE RISK OF PANCREATIC INFECTION

MEROPENEM:

A subsequent randomized controlled trial that used meropenem 1 gram intravenously every 8 hours for 7 to 21 days stated no benefit

ERCP:

Early ERCP (endoscopic retrograde cholangiopancreatography), performed within 24 to 72 hours of presentation, is known to reduce morbidity and mortality.[47]

The indications for early ERCP are as follows :

Clinical deterioration or lack of improvement after 24 hours

Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen

The disadvantages of ERCP are as follows :

ERCP precipitates pancreatitis, and can introduce infection to sterile pancreatitis

The inherent risks of ERCP i.e. bleeding

It is worth noting that ERCP itself can be a cause of pancreatitis.

Surgery

Surgery is indicated for

(i) infected pancreatic necrosis

(ii) diagnostic uncertainty

(iii) complications.

COMPLICATIONS Systemic complications

1. Metabolic

Hypocalcemia, hyperglycemia, hypertriglyceridemia

Respiratory

Hypoxemia, atelectasis, Effusion, pneumonitis, Severe acute respiratory syndrome (SARS) Renal Renal artery or vein thrombosis Renal failure

Circulatory Arrhythmias Hypovolemia and shock myocardial infarct Pericardial effusion vascular thrombosis

Gastrointestinal

Gastrointestinal hemorrhage from stress ulceration;

gastric varices (secondary to splenic vein thrombosis)

Gastrointestinal obstruction

Hepatobiliary

Jaundice

Portal vein thrombosis

Neurologic Psychosis or encephalopathy (confusion, delusion and

coma)

Cerebral Embolism

Blindness (angiopathic retinopathy with hemorrhage)

Hematologic Anemia

DIC

Leucocytosis

Dermatologic Painful subcutaneous fat necrosis

FEATURES OF ACUTE VIRAL HEPATITIS

FEATURES OF LEPTOSPIROSIS

MCQ 1

WHICH OF THE FOLLOWING IS NOT A CRITERIA IN RANSON SCORING OF ACUTE PANCREATITIS?

S/LDH

S/CA

S/LIPASE

HCO3 LEVEL

TLC COUNT

MCQ 2

WHICH OF THE FOLLOWING IS THE GOLD STANDARD INVESTIGATION FOR DIAGNOSING SEVERE/NECROTIC PANCREATITIS?

USG ABDOMEN

XRAY ABDOMEN

TRIPLE PHASE CT ABDOMEN

PET SCAN

CATSCAN

MCQ 3:

FOLLOWING IS THE MOST SPECIFIC INDICATOR OF PANCREATIC INJURY?

S/LDH

S/TRIGLYCERIDE

S/LIPASE

S/AMYLASE

HCT