35 F with pain abdomen

 

35 year old with pain abdomen

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CHIEF COMPLAINTS :

 

35 year old female who is a wig maker and goes to part time work in paddy and cotton field’s presented to the Emergency department with acute history of pain abdomen & vomiting’s since 4 days  

 

INTRODUCTION INTO BIOPSYCHOSOCIAL ASPECTS OF THE CASE:

 

Activities of daily leaving before illness:

 

Patient was apparently asymptomatic 7 years (2016) back where here daily routine before illness was waking up at 4 am after cleaning house and fresh-up herself, prepare food for the family. She used to have IDLI, DOSA, RAAGI JAVA as her breakfast and take rest for few minutes and enjoys working for family household needs like cooking, laundry, cleaning home etc. she prepare dinner and get to sleep by 10pm.

 

History of presenting illness:

 

Down the line 7 years back in 2016 while she was going in auto she was having conversation with driver (cousin) and met with an road traffic accident where auto was hit by lorry from back. She had sustained injury to her head with minor superficial injuries on face, fear of impending doom ( first psychological impact ) with no loss of consciousness, no history of headache , no history of vomiting’s, then she was shifted to nearest medical care and was incidentally diagnosed with type -2 Diabetes mellitus.

After an year in 2017 her husband developed severe headache for 3 months and attaining medical check-up she was counseled that her husband had some lesions in brain (described as blood clots) and he will not survive for more than 3-6 months (with no motor deficits) and he passed away after 2 months (second psychological impact).

Following demise of her husband her life was taken another path where here daily routine was scheduled to earn for living (third psychological impact with associated social factors).

 

Impaired activities after death of her husband:

 

Wakes up around 4am in the morning, gets ready for work with frequent skipping of breakfast compared to past. She starts her work at 8-9am sell ornaments, sometimes work in paddy fields (for planting and other farming work). She get back to home by 11:00 am have some snacks and look after her elder daughter while she was pregnant and younger daughter who is pregnant now. Household work, and sits at a retail shop or play with her grand-daughter. She bags around 4000-6000 per month with net savings of 500-700 rps/- per week approximately.

She used to raise money 10000-20000 based on need at local groups for her daughters health check-ups, sons college fees and or daily household needs which was cleared by her savings.

She developed frequent burning sensation in her chest localized to epigastric region associated with bloating, belching and altered bowel habits (constipation with once in 2 days since last few months) 

 

Possible stressors and outcomes:

 

Impaired daily activities

Physical and emotional stress

Social stress (financial burden)

Altered food and bowel habits

Dyspepsia and frequent use of antacids.

 

Acute History of presenting illness:

 

Now, presenting with complaints of pain abdomen originated at left hypochondrium and lumbar region (VAS 7 score) then became diffuse in type over 10 to 12 hours (VAS 10

Worst pain she ever had), squeezing type of pain with occasional coliky type, associated with vomiting’s 2-3 episodes non bilious , non-projectile, non-blood tinged with food particles as content. Passing stools small amount (as fecal pellets of goat - described by patient) didn’t pass flatus since 2 days. 

history of bloating, belching since 5 years using antacids. 

Passage of hard stools since 2 months (Bristol stool chart - type 1) 

 

MARRIAGE & OBSTETRIC HISTORY

 

Married at the age of 17 years , non-consanguineous. 

FIRST child at 18 years - death of the first child at 24years due to varicella zoster. 

2nd child at age of 21 years - gave  birth to female child , now married 

3rd child at the age of 23 years -gave birth to female child , now married 

4th child at the age of 24years - gave birth to male child currently 10th class.

 

PERSONAL HISTORY:

 

Mixed diet, appetite reduced

Constipation since 5 months

NON SMOKER AND NON ALCOHOLIC

 

FAMILY HISTORY:

 

Mother is hypertensive and expired due to cerebrovascular accident and post stroke complications after 6 months.

 

DRUG HISTORY: weekly she used to take 2-3 sachets of ENO (antacids)

 

 

 

 

AT PRESENTATION: 

Patient is conscious, coherent and Co-operative well oriented with time, place and person.

 

VITALS AT PRESENTATION:

 

Febrile to touch 99.1 F 

Blood pressure: 110/80mmhg in right upper arm supine position.

Pulse rate: 119 per minute, regular, normal volume 

Respiratory rate: 24 cycles per minute (pain induced tachycardia)

Room air saturation: 92%

 

GENERAL EXAMINATION:

 

Looks grossly dehydrated with sunken eyes, dry oral mucosa and tongue with delayed capillary refill time (more than 3 seconds)




Pallor present

bilateral pitting type of pedal Edema present with scratch marks on both lower limbs (pruritus due to possible diabetic dermopathy)  

No icterus, cyanosis, clubbing, lymphadenopathy.

She used to colour her hair since 8 years (early whitening of hairs at 28 years – probable zinc and other nutritional deficiencies)

 

SYSTEMIC EXAMINATION:

 

EXAMINATION OF THE ORAL CAVITY

NO Oral thrush, NO tonsilar enlargement & pharyngeal deposits, NO post nasal drip, NO fetor hepaticus, Fair oral hygiene, no dental caries and no gum hypertrophy.

 

ABDOMEN:



 





INSPECTION:

1. Shape – distended-uniform

2. Flanks – full

3. Umbilicus – central, Shape-slit like and nodules.

4. Skin – stretched, no scars & sinuses, striae present, scratch marks.

5. No Dilated veins – front/back

7. Movements of the abdominal wall,NO visible gastric & intestinal peristalsis.

8. Hernial Orifices - normal

9. NO Renal angle tenderness

Nasogastric tube aspirate 200ml since admission.

 

PALPATION:

Superficial Palpation – Tenderness present at left hypochondrium and lumbar region, no local rise in temperature.

Deep Palpation

1.       Liver: inferior edge palpable, smooth non nodular.

2.       Spleen non palpable and non-tender when palpated in the Left Hypochondrium.

3.       Kidney non-tender and non palpable in the Right/Left Lumbar.

4.       Abdominal Girth - 79cms

5.       Distance between the Xiphisternum-Umbilicus and Umbilicus-Pubic Symphysis equal 17 cms.





6.       No Murphy’s Punch/Renal angle tenderness.

 

PERCUSSION:

1. Puddle’s sign present suggestive of mild fluid collection in abdomen.

2. Percussion of Liver for Liver Span - 13cms

 

AUSCULTATION:

1. Bowel sounds – sluggish

2. No Bruit – Aortic, Hepatic, Renal Bruit

3. No Venous Hum.



 

OTHER SYSTEMS EXAMINATION:

 

CARDIOVASCULAR SYSTEM:

No raised Jugular venous pressure

Apex beat in 5th Intercostal space on left mid clavicular line

S1 and s2 heard. NO murmurs.






 

EXAMINATION OF RESPIRATORY SYSTEM:

No tracheal deviation

Respiratory movements are bilateral symmetrical

Resonant percussion in all lung field’s

Normal vesicular breath sounds.



 

EXAMINATION OF NERVOUS SYSTEM:

Higher mental functions intact

All Cranial nerves on both sides are intact

No motor deficits

Sensory system :

Fine touch - absent below both ankles

Vibration - delayed in both lower limbs ( 6sec at ankle, 8 sec at knee ) and upper limbs ( 9sec in upper limb )

Gait normal

 

PROBLEM STATEMENT:

A 35 year old diabetic female with acute history of diffuse pain abdomen with nausea followed by vomiting and peripheral neuropathy.

 

Differentials:

1.       Acute intestinal pseudo-obstruction (ogilvie syndrome)

2.       Gastroesophageal reflux disease (GERD/?LAX lower esophageal sphincter)

3.       Possible Acute pancreatitis (extends from hilum of spleen to epigastrium)

4. Peripheral neuropathy secondary to Diabetes 


Gastroenterologist consultation was taken : 

Advised for IgG4 antibodies , ANA and MRCP.


Investigations : 









Diagnosis:

Hypertriglyceridemia induced acute pancreatitis with type 1 diabetes mellitus 

Acute colonic pseudo obstruction ( Ogileve syndrome - resolved )

Gastroesophageal reflux disease

Diabetic peripheral neuropathy and 

Acute kidney injury ( prerenal ) secondary to Dehydration and pancreatitis

Indirect hyperbilirubinemia secondary to (?enzyme defecf / hemolysis)


Discussion : 

How is triglyceride levels associated with pain abdomen in our case. .??

mon.[1] Metabolic, structural, and iatrogenic causes account for 20 – 25% of the cases.[2] Hyperlipidemia in the form of hypertriglyceridemia or chylomicronemia, although less frequent, is one of the well-accepted underlying causes of acute pancreatitis in 7% of the cases — the most common after gall stones and alcohol.[3] Typically hypertriglyceridemia-induced pancreatitis occurs in a patient with a pre-existing lipid abnormality, along with the presence of a secondary precipitating factor (e.g., poorly controlled diabetes, alcohol or medication). The triglyceride levels of more than 1000 to 2000 mg / dl in patients with type I, III, IV, and V hyperlipoproteinemia (Friedrickson's classification) is the identifiable risk factor.[4] Genetic factors determine over 60% of the variability in serum lipids.[5] The secondary causes of hypertriglyceridemia have to be ruled out. Most patients can be effectively treated with the existing drug therapy. Heparin and insulin have a role to play in the treatment.[6] Other novel modalities include plasma exchange and lipid aphaeresis.[7] Here we report a lady presenting with recurrent pancreatitis, with features of hyperlipidemia, and review the literature for pathogenesis and management of hyperlipidemia.
The association between acute pancreatitis and hyperlipidemia is well known, both as a precipitant and as an epiphenomenon.[8] The coexistent medical conditions such as diabetes should prompt further workup.[9] Hypertriglyceridemia can be primary in less than 5% of the cases, due to genetic causes and more often secondary to other causes like diabetes, obesity, pregnancy, excess carbohydrate intake, hypothyroidism, alcohol, hepatitis, sepsis, renal failure, and drugs like estrogen, glucocorticoids, β blocker, bile acid binding resins, thiazide, tamoxifen cyclosporine protease inhibitors, and isotretinoin.[10]
Link With similar case like ours

[4/26, 10:52 AM] saicharankulkarni: Probable final diagnosis

Hypertriglyceridemia induced acute pancreatitis with Latent auto immune diabetes ( LADA ) 

Acute colonic pseudo obstruction ( Ogileve syndrome - resolved )

Gastroesophageal reflux disease

Diabetic peripheral neuropathy and 

Acute kidney injury ( prerenal ) secondary to Dehydration and pancreatitis

Indirect hyperbilirubinemia secondary to (?enzyme defecf / hemolysis)

[4/26, 11:51 AM] Dr Rakesh Biswas Sir Hod Gm Kam: The most important part of any diagnosis that needs to be mentioned is the duration of each 

How long diabetes? 

Why LADA? 

How can you have both pancreatitis and Ogilvie's?
[4/26, 11:51 AM] Dr Rakesh Biswas Sir Hod Gm Kam: What about the rest of her triopathy?

[4/26, 1:25 PM] saicharankulkarni: Nephropathy - awaited for urinary protein and creat
Retinopathy - Not present
Neuropathy - glove and stock pattern. ( Absent vibration and fine touch on foot )

[4/26, 1:32 PM] saicharankulkarni: 

In context of differentiating LADA from type 2Dm 
http://drsaicharankulkarni.blogspot.com/2023/04/35-f-with-pain-abdomen.html


Latent autoimmune diabetes in adults (LADA) is considered a subgroup of type 1 diabetes and is often misdiagnosed because of a lack of both awareness and standardized diagnostic criteria (1–3). LADA is characterized by adult-onset diabetes and circulating autoimmune antibodies; thus, patients may present clinically with characteristics of both type 1 and type 2 diabetes (2–5). Typically, the clinical features of type 1 diabetes seen in LADA include a lower BMI compared to what is typical in type 2 diabetes and autoimmunity against one or more of the following antibodies: islet cell autoantibodies (ICA), autoantibodies to glutamic acid decarboxylase (GAD), tyrosine phosphatase–related islet antigen 2 (IA-2), and insulin autoantibodies (IAA) (4,5). The characteristics of type 2 diabetes that may present in LADA include older age at onset and insulin resistance or deficiency. Characteristics of LADA tend to include an intermediate level of β-cell dysfunction between those in type 1 and type 2 diabetes, faster decline of C-peptide compared to type 2 diabetes, and a level of insulin resistance that is comparable to type 1 diabetes (4). β-Cell decline is variable in LADA, as measured by C-peptide levels

Patient complained worsening of pain abdomen, emergency surgery referal was taken and advised for MRCP
 So patient is refered to higher center for MRCP.

Discoloration noted at left hypochondrium and lumbar region.


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