26 years old male presented with pain abdomen and vomitings

Hi I'm Saranya, 3rd sem student .This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent.

 

Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 

This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box.

CHEIF COMPLAINT

 Pain abdomen after taking food since 1 day

 Vomitings since 3 days

Loss of appetite

Burning mituration

Cold and cough

SOB

HISTORY OF PRESENT ILLNESS-

A 26 year old male , car driver by occupation came with abdominal pain and vomitings of 3 episodes which is bilious,non blood tinged,No fever and has cold and cough

He is apparently asymptomatic 4 months back,then he took alcohol regularly for 1 week, then started developing pain abdomen associated with vomitings for which he was admitted admitted in hospital for 1 week and diagnosed as acute pancreatitis then he was fine . Again started consumption of toddy regularly and then 1 day back started pain abdomen in EPIGASTRIC REGION not received by medication and associated with vomitings which has 3 episodes, burning mituration.

On examination tenderness present on RIGHT HYPOCHONDIUM

Past History

No h/o HTN, TB, CAD, Asthma

Personal History

Diet: mixed

Appetite: normal

Sleep: adequate

Bowel and bladder: regular 

Habits: Regular TODDY consumption

Family history

Not significant

General Examination

The pt is conscious on examination

Well oriented to time, place and person

Moderately built and moderately nourished

Pallor – absent

Icterus - absent

Cyanosis - absent

Clubbing – absent

Lymphadenopathy - absent

Edema – absent 

Temperature – Afebrile

HR – 70bpm

RR – 18 cpm

SpO2 – 97%

Systemic Examination

CNS:

 Conscious, oriented to time place and person.

Patient is drowsy but arousable

 Speech: normal

 Behavior: normal 

Memory: Intact.

 Intelligence : Normal

 Lobar Functions : Normal.

 No hallucinations or delusions.

 

Cranial Nerve Examination: All cranial nerves are functionally normal

Motor system examination: Normal

CVS: 

AUSCULTATION 

Rate is normal

Rhythm is regular

S1, S2 heard, No murmurs

Respiratory: 

Inspection:

Upper respiratory tract - oral cavity, nose & oropharynx appears normal.

Chest appears Bilaterally symmetrical & elliptical in shape

Respiratory movements appear equal on both sides and it's Abdominothoracic type.

Trachea central in position & Nipples are in 4th Intercoastal space

No signs of volume loss

No dilated veins, scars, sinuses, visible pulsations.

ABDOMEN

Obese in shape, soft, non-tender, bowel sounds heard, no hepatosplenomegaly

INSPECTION

➤Shape - obese , with no distention.

➤Umbilicus - Inverted

➤Equal symmetrical movements in all the quadrants with respiration.

➤No visible pulsation, peristalsis, dilated veins and localized swellings

PALPATION

TENDERNESS PRESENT ON RIGHT HYPOCHONDIUM 

 AUSCULTATION

Bowel sounds present

INVESTIGATIONS

MEDICATIONS

                        ACUTE PANCREATITIS

Pancreatitis is inflammation of the pancreas. The pancreas is a long, flat gland that sits tucked behind the stomach in the upper abdomen. The pancreas produces enzymes that help digestion and hormones that help regulate the way your body processes sugar (glucose).

Pancreatitis can occur as acute pancreatitis — meaning it appears suddenly and lasts for days. Some people develop chronic pancreatitis, which is pancreatitis that occurs over many years.

 Where is anatomical location of this patient's problem? (related to Macroanatomy) ?

 In the Pancreatic acinar cells of the patient is defective due to various causes like alcohol, matastasis, gallstones, high triglycerides etc

Why is the patient having this problem? (related to microanatomical pathogenesis as well as macro-social environmental events influencing it) 

The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes. In biliary acute pancreatitis, outflow obstruction with pancreatic duct hypertension and a toxic effect of bile salts contribute to disruption of pancreatic ductules, with subsequent loss of extracellular compartmentation. Alcohol induces functional alterations of plasma membranes and alters the balance between proteolytic enzymes and protease inhibitors, thus triggering enzyme activation, autodigestion and cell destruction. Once the disease has been initiated, the appearance of interstitial edema and inflammatory infiltration are the basic features of acute pancreatitis. The accumulation of polymorphonuclear granulocytes in pancreatic and extrapancreatic tissue, and the release of leukocyte enzymes play an essential role in the further progression of the disease and in the development of systemic complications. Activation of different cascade systems by proteolytic activity, and consumption of alpha 2-macroglobulin further characterize the severe clinical course of acute pancreatitis.

Macrosocial environmental factors

Excessive alcohol consumption. Research shows that heavy alcohol users (people who consume four to five drinks a day) are at increased risk of pancreatitis.

Cigarette smoking. Smokers are on average three times more likely to develop chronic pancreatitis, compared with nonsmokers. The good news is quitting smoking decreases your risk by about half.

Obesity. You're more likely to get pancreatitis if you're obese.

Diabetes. Having diabetes increases your risk of pancreatitis.

Family history of pancreatitis. The role of genetics is becoming increasingly recognized in chronic pancreatitis. If you have family members with the condition, your odds increase — especially when combined with other risk factors.

What are we doing about it? (pharmacological and non pharmacological interventions)

Pharmacological interventions:

NBM till further order

IVF -NS AND RL

TRAMADOL -IV

Zofer 4mg

T.Pancreo flat polo

Pan 40 mg

Non pharmacological interventions 

Conservative plan of care

2D echo

ECG

Serum amylase ,lipase 

Lft

Rft

Hemogram

CXR