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Case Discussion

History

36 year old male navy officer

surgical casualty ward

with one day history of

fever

epigastric pain- radiating to back

sever nausea and vomiting

h/o GORD symptoms

nonsmoker

teetotaler

Examination

severe pain +

Ill looking

Febrile

Not pale

Not icteric

Examination

BP 90/60 mmHg/ Pulse 102/ CRFT< 2s

Lungs – bi-basal reduced air entry

L>R Spo2- 96% on air

Abdomen – slight distension

mild tenderness

What are the differential

diagnoses?

1. Acute cholecystitis

2. Ascending cholangitis

3. Dengue/ viral fever with hepatitis

4. Acute pancreatitis

5. PUD

6. Acute intestinal obstruction

7. Diabetic ketoacidosis

What laboratory

investigations would

you choose?

Initial investigations

FBC - Hb -11 mg/dl

WBC -11,000/mic.l(N-86%)

Platelets-110,000/mic.l

UFR- few pus cells only

CBS- 145mg/dl

Other lab tests

Serum amylase

Serum lipase level

Serum amylase in our patient-

35 iu

would imaging be helpful?

Imaging of the abdomen

X-ray-erect

NCT

CECT

MRI

US Scan

Us scan abdomen was done

Moderate amount of free

fluid +

Emergency laparotomy was

done in the night

Findings???

Saphonification of omental

fat tissue

Findings –small amount of free fluid

bowel, appendix and liver normal

Saphonification of omentum noticed

Abdomen was closed with a drain

Patient was taken to the ICU

BISAP score for pancreatic

mortality

B – BUN > 25mg/dl 0 – 0.2%

I – impaired mental status 1 – 0.6%

S – SIRS criteria ( 2 or more ) 2 – 2%

A - > 60yrs 3 – 5-8%

P- Pleural effusion present 4 – 13-19%

5 – 22-27%

Intensive care management

Hydration

Cardiovascular support

Ventilatory support

Treat infections

Nutrition

DVT prophylaxis

Pain management

ERCP

Is there a specific

management to improve

outcome in ASP ?

Early aggressive intravenous

hydration

How early..

Within first 24 hrs

Patient not responding to aggressive

therapy early(6-12hrs) may not benefit

continuing.

How aggressive?

250-500ml per hour(5-10ml/kg/hr)

Caution in cardiac and/or renal

disease

Which fluid..?

Ringer’s lactate is better than 0.9% saline

Better electrolyte balance

Improved outcome

pH balance

Causes and effects of

hypovolaemia

Multiple causes

Extravasation

Vomiting

Reduced oral intake

Respiratory and evaporator losses

Hypovolaemia activates a vicious cycle that lead to

pancreatic necrosis worsening the clinical condition.

If the patient goes in to shock more

rapid fluid boluses may be needed

under invasive cardiac output

monitoring

Goal directed fluid theraphy

How do you monitor initial

fluid responsiveness?

Goals are to…

Decrease haematocrit

Decrease BUN

Normal creatinine

UOP≥ 0.5ml/kg

Advanced monitoring

Stroke volume variation

CO moitoring

How to determine fluid requirement in patients with

persistent organ failure despite early aggressive therapy

Non responders

Surviving sepsis

CVP line inserted and fluid

resuscitated

During the ICU stay

BP 85/45 mmHg(MAP-58 mmhg)

Pulse rate 130bpm

Vasoactive drugs

Theoretically all vasoactive drugs can

reduce splanchnic blood supply(esp.

phenylephrine) and increase the risk of

necrosis

But MAP should be ≥65 to maintain

organ perfusion

Noradrenalin is the first choice

Noradrenaline started

During the ICU stay

Low oxygen saturation spo2 92%

CPAP started

CPAP 8 and FiO2 50%

oxygenation improved to SpO2 98%

Later patient deteriorated despite NIV with

high O2 ,and invasive ventilation done

with lung protective measures

During the ICU stay

Arterial blood gas analysis;

pH 7.3

Pao2 55mmHg

Paco2 32 mmHg

Hco3 16 mmol/l

Be – 10 mmol/l

SaO2 88% with high flow O2

During the ICU stay

US Scan chest– small, bilateral pleural effusions,

left>right

Chest X-ray- supine x-ray

no definite effusion

lung fields not clear

How to improve oxygenation?

Ventilatory strategy

Majority of SAP develop ARDS

Lung protective ventilation according to

ARDSnet

Ventilatory care bundle

4. Analgesia

morphine infusion 2-3mg /h

fentanyl as sos boluses

5. Antibiotics

What is the

antibiotic policy in

AP?

Extrahepatic infection should be treated

accordingly

Routine use of prophylactic antibiotics in

the early stage SAP is not recommended

Antibiotics should be given

Patients with confirmed infected

necrosis

Patients fail to improve after 7-10days

after hospitalization

SIRS that occur early in AP may

indistinguishable from sepsis syndrome

CT FNA is the only way to distinguish

infected necrosis from sterile necrosis.

60% of AP develop sepsis

Which antibiotic…

Carbapenems

Quinolones

metronidazole

Prophylactic antifungal agents is not

recommended.

6.Nutrition

Are we going to feed

this patient?

NBO is pre historic…

Bowel rest and TPN increase,

mucosal atrophy and bacterial translocation

Catheter-related blood stream infections

Morbidity and mortality

Early enteral nutrition,

decrease hospital stay

Decrease infective complications

Decrease morbidity and mortality

Which route

Oral

NasogastricSafe

no significant increase in aspiration risk

Easy tube placement

Nasojejunal

Feeding jejunostomy

7.DVT prophylaxis

Only TED stockings were used in addition

to the general measures

Anticoagulants not used due to high INR

What is the role of

antisecretory drugs?

Role of drug therapy in AP

No proven benefit in

Gabexate – anti-protease

Octeotride – anti-secretory

Bladder pressure was

monitored

60% to 80% of SAP can develop intra

abdominal hypertension

intra-vesical pressure should be

monitored frequently

6hrly in all the patients with SAP

4hrly in IAH

Second week CECT abdomen – necrotic

pancreatitis – conservatively managed

After thre weeks patient was

extubated

Off noadrenaline

Feeding established

Sent to ward

Thank You!