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..
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)
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
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
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 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
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
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
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
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