59F chronic pancreatitis , Dm ( 3c)

57 year old female gardener resides near Sanghi ( hayathnagar)

Presented with C/o fever since 3 days, high grade, continuous, with chills, relieved with medication, 

pain in epigastrium since 3days, non radiating, not associated with burning, belching, associated with 

one episode of vomiting, with food content, non bilious, non projectile, non blood stain

No h/o chest pain, breathlessness, giddiness, palpitations, orthopnea,pnd,cough, cold, burning micturition, loose stools

She's second born child ,whose father was toddy tree climber and has daily habit of consumption of toddy.

She was made to start toddy consumption at very young age of 4-5years considering it to be good for health

And consumes daily 1glass of toddy thrice everyday for 15 years 

Works as farmer from age of 22 years at chittaluru near chitiyal ,Married and moved to hyderabad near seethaphalmandi.

Stopped consuming toddy after marriage 

And stopped working for some time after her marriage.

At age of 23 years- patient conceived spontaneously ,had regular ANC done , was anaemic .LSCS was done at term i/v/o ? Post dated ? CPD and was discharged with both healthy Mother and child after a week 

She had decreased appetite , easy fatiguability ,occasional fever with joint pains ( once/month) associated with morning stiffness for 20min ,went to local practitioner and had temporary symptomatic relief with painkillers,antacids .

Joints involved - knee,elbow ,wrist occasionally small joints of hand which relieved with rest.

After an year she conceived spontaneously and was on regular medication and Followup 

On her 8th month pregnancy - flight with husband ,who kicked her back .20 days later when taken to local hospital during her labour .Emergency LSCS was done , child expired after 24hrs birth( ?meconium aspiration)

Patient continued to develop these symptoms of fever with joint pains , pain abdomen ( aggrevated with food Intake) and was consuming medications with no adequate relief 

3years later - 27 years of age 3rd child delivered ,FTD, LSCS.

She started working as gardener, animal rearer.

Continued to develop these symptoms ,was neglected by her husband.

At 34 years age- 

Recurrent fevers, increased appetite,thirst, easy faituagibility for 2 months

Taken to private clinician and found to have high GRBS(? Around 300s)

Was suggested Diabetic Diet and Oral hypoglycemic drugs.

Patient used them for 3 years with no improvement in her symptoms and later went to diabetologist in dilsukhnagar

Where she was started on insulins 

She also complained of blurring of vision during the same and diagnosed to have ? Diabetic retinopathy and refractive error started using glasses.

Patient continued using medications and was asymptomatic until 8 years back

She was brought to KIMS with pain abdomen, shortness of breath , decreased responsiveness found to have increased sugars ? DKA was treated with insulin and fluids .

1 year later - 

Patient developed severe pain abdomen at epigastric region 

Squeezing type aggrevated with food Intake relieved with medication

Associated with vomiting - non bilious non projectile , aggrevated with food Intake 

Taken to private practitioner and scan was done showing ? Pancreatitis 

She was then taken to KHL - confirmed diagnosis and was told to have Stones in her pancreas

And was put on medical management .

Despite all these patient developed symptoms and were progressively increasing which started to hamper her daily routine and work 

And stopped working 

1 year later - similar episodes with increased frequency ( once / week)

Associated with increased joint stiffness and presented to KIMS . Pain abdomen , vomiting and difficulty in shoulder movement ( overhead abd) managed conservatively. 

2 years back - presented with severe pain abdomen, weight loss( approx 7kgs-8kgs), vomiting ( 4-5episodes/day) 

Was taken to Osmania Endoscopy MRCP was done 

They suggested Pancreaticojejunostomy 

( to reduce the sugars and recurrent pancreatitis episodes- as per attenders)

After a month surgery was done in OMC. 

Post operatively she was hail and healthy ,with prior insulin requirement (HAI 20-14) 

Post operative (HAI+ mixtard 14-12)

And was asymptomatic until 8 days back 

[17/04, 11:55] Dr Rakesh Biswas Sir HOD: Just saw this patient in a new light in the wards thanks to @⁨Dr.Deepika Ch⁩ 

Apparently type 3 diabetes is what she has! 

We had even made a fascinating hypothesis from her diabetes during her last admission in December but now perhaps it was wrong in her case although it could still be true in general for the relation between adiposity, sarcopenia and diabetes.

Has had a pancreaticojejunostomy three years back as a drainage procedure for prior diagnosed chronic ductal obstructive pancreatitis!

Hopefully Deepika will share the details now

[18/04, 20:45] Dr Aditya Gmed Pgy3: Cause of Chronic Pancreatitis?

[18/04, 20:46] Dr Aditya Gmed Pgy3: Any history of exocrine insufficiency too? Surely it may have preceeded the Endocrine insufficiency?

History appears to be suggestive of LADA too.

[18/04, 20:48] Dr Aditya Gmed Pgy3: @⁨Dr Rakesh Biswas Sir HOD⁩ Can hemochromatosis (either primarily or secondary to alcohol abuse) do this? Joints and pancreas?

[18/04, 20:57] Dr.Deepika Ch: Sir my differentials are-

1. Alcohol (toddy consumption)

2. Autoimmune mediated ( AIP)

3. Due to Recurrent acute pancreatitis .

[18/04, 20:58] Dr Aditya Gmed Pgy3: Yes i agree but why has there never been exocrine insufficiency preceding the Endocrine insufficiency? Quite unusual isn't it?

[18/04, 20:59] Dr Aditya Gmed Pgy3: Unless something is directly attacking the islets, such as LADA?

[18/04, 21:01] Dr.Deepika Ch: Yes sir

She did complain of bloating sensation especially after consumption of protein rich diet 

And occasional sticky stools too sir ( ? Steathorrea) 

These symptoms were present during the time of diagnosis of diabetes sir.

[18/04, 21:03] Dr Aditya Gmed Pgy3: Okay. Are they due to Diabetic Enteropathy / Hyperglycemia or Osmotic Diarrhea / Exocrine insufficiency of Pancreatitis

How would you differentiate between the 3? Also make no mistake SIBO is 1.3x more prevalent among diabetics than those who don't have it.

How would you differentiate among these 4?

[18/04, 21:28] Dr Rakesh Biswas Sir HOD: Regardless of what the relatives were told, can you review the literature and share the indications for pancreatico jejunostomy?

[18/04, 21:40] Dr.Deepika Ch: Diabetic gastroparesis - 

Nausea,vomiting ,early satiety ,post prandial fullness

Decreased gastric motility

Investigations-

Gastric emptying by scintigraphy

Breath test

Exocrine insufficiency of pancreas-

Steathorrea 

Weight loss 

Bloating

Albumin and vitamin deficiencies- a,d,e,k

Investigations-

Secretin / secretin-cck stimulation tests

Fecal elastase

Hyperosmolar diarrhea-

Bulky stools 

Increased stool osmotic load decreases with fasting

[18/04, 21:40] Dr.Deepika Ch: Ohk sir

[18/04, 21:47] Dr Aditya Gmed Pgy3: And the much more likelier one SIBO?

[18/04, 21:57] Dr Aditya Gmed Pgy3: Has your Clinical examination been helpful in including or excluding any of these differentials?

[18/04, 22:39] Dr.Deepika Ch: SIBO-

Cc-

bloating

Flatulence 

chronic watery diarrhea. Steatorrhea and weight loss from fat malabsorption 

Vitamin defeciencies- Vit B12,Vit D

Causes- DM

gastric motility disorders

IBS,

Pancreatic insufficiency

Post radiation 

Hypothyroidism

Investigations-

positive carbohydrate breath test or a bacterial concentration of more than 1000 colony-forming units/mL in a jejunal aspirate.

macrocytic anemia, low B12, thiamine, and niacin levels, elevated folate, vitamin K levels, and increased fecal fat content

[18/04, 22:48] Dr.Deepika Ch: Sir the patient had

Tenderness in epigastrium 

With early satiety and post prandial fullness 

With no steathorrea now sir

Bowel sounds - 4/min 

So I'm thinking patient to have diabetic gastroparesis sir

[18/04, 22:49] Dr Aditya Gmed Pgy3: Okay. How would you explain the Endocrine insufficiency preceding the exocrine insufficiency? Any literature on that?

[18/04, 22:50] Dr Aditya Gmed Pgy3: Assuming this is chronic pancreatitis. Vaguely remember reading skme literature on both IgG4 and LADA closely mimicking Chronic Pancreatitis.

Food for thought.

[18/04, 22:55] Dr.Deepika Ch: Will review and update sir 

Sir could it be that the patient is on pancreatin would her symptoms have been alleviated now?

[18/04, 22:56] Dr Aditya Gmed Pgy3: Oh did she have a past history of documented exocrine insufficiency then?

[18/04, 22:58] Dr.Deepika Ch: She was put on these enzymes post surgery .

But no documentation was available sir

[19/04, 01:09] Dr.Deepika Ch: it was brought to light that some patients with AIP experienced pancreatic stone formation, pancreatic atrophy, and/or irregular dilatation of the MPD over a long-term course[14, 29–38]. Such imaging findings mimicked those of chronic pancreatitis, suggesting that patients with AIP could progress to this state.

Eight patients (19%) developed pancreatic calcification. Because 6 of 11 patients (54.5%) who relapsed had detectable calcification, pancreatic calcification in AIP became significantly associated with relapse patients in comparison with non-relapse patients

Pancreatic stone disease was again significantly more frequent in the recurrence group (7/21, 33%) than in the non-recurrence group (2/30, 7%) (p = 0.014)

.We nonetheless maintain that in early stage AIP, intensive PSL therapy has the potential to prevent pancreatic stone formation as well as the progression to chronic pancreatitisMore detailed analyses of maintenance therapy and follow-up regimens are needed.

We measured the serum values of IgG4 in 175 patients with confirmed chronic pancreatitis who had been diagnosed before 1995, which was the year when the concept of AIP was first proposed, and uncovered raised serum IgG4 in 13 patients (7.4%)

During the course of the above study of 73 patients with AIP, progression to chronic pancreatitis in terms of the revised JCDC was seen in 16 patients (22%), who were defined as the progressio group, as compared with the remaining 57 non-progression group patients who did not develop chronic pancreatitis. 

progression rate to chronic pancreatitis was 10% at 36 months, 20% at 100 months, and 30% at 124 months. Advancement to chronic pancreatitis was not observed after 124 months, suggesting that the window for disease development was within 10 years of follow-up. 

https://ojrd.biomedcentral.com/articles/10.1186/1750-1172-9-77

[19/04, 08:47] Dr.Deepika Ch: lateral pancreaticojejunostomy provided pain relief, had a low morbidity rate, and no early postoperative deaths, long-term outcome was poor based on the patient's health status, continued alcohol and narcotic use, employment status, subsequent hospitalization to treat recurrent pancreatitis or its complications, subsequent operations required for complications of chronic pancreatitis, and postoperative deaths related to comorbid medical conditions or complications of chronic pancreatitis.

Post operative health status

Good - 24%

Fair- 31%

Poor- 45%

Rehospitalisation for recurrent attacks- 40%

Death - 26%

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1243174/?page=5

[19/04, 08:51] Dr.Deepika Ch: chronic pancreatitis, longitudinal pancreaticojejunostomy (LPJ) is the treatment of choice for patients with a dilated main pancreatic duct (MPD) without an inflammatory mass in the pancreatic head. This procedure is associated with low morbidity and mortality rates. Immediate and lasting pain relief is reported in 80% (range, 42%–100%) of patients with a follow‐up of 62 mo (range, 15–110 mo). 5 , 6 , 7 It is a relatively simple, safe, and effective surgical procedure for patients with dilated MPD

surgical indication of LPJ after PD was dilation of the main pancreatic duct (MPD ≥ 5 mm) due to anastomotic stricture in patients with recurrent obstructive pancreatitis or rapid deterioration of glucose tolerance. Obstructive pancreatitis was defined as acute onset of severe epigastric and/or back pain with serum pancreatic amylase activity at least three times greater than the upper limit of normal and characteristic findings of acute pancreatitis on imaging studies. Rapid deterioration of glucose tolerance was defined as a rapid increase in serum hemoglobin (Hb) A1c levels (≥2.0%) over a few mo (2–6 mo).

median follow‐up period of 39 mo (range, 4–126 mo) after LPJ, preoperative symptoms improved in 16 patients (89%). Nine of 10 patients (90%) with obstructive pancreatitis achieved complete relief of pain. However, one patient achieved no pain relief. One patient required readmission due to recurrent pancreatitis during the follow‐up period. All nine patients who had rapid deterioration of glucose tolerance had improved glucose control and endocrine function. The changes in serum HbA1c levels before and after LPJ in these patients are shown in Figure 3. Serum HbA1c levels rapidly increased before LPJ and decreased after LPJ. Mean doses of daily insulin before and after LPJ were 11.6 ± 3.3 units and 3.4 ± 4.3 units, respectively. The daily insulin requirement significantly decreased after LPJ (P = .0239). Although seven patients required insulin before LPJ, four were free of insulin after LPJ. One patient required re‐LPJ 7 mo after LPJ owing to increased HbA1c levels (Figure 3). Although the patient required 20 units of daily insulin just before re‐LPJ, the patient was free of insulin after re‐LPJ.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9130871/#:~:text=In%20chronic%20pancreatitis%2C%20longitudinal%20pancreaticojejunostomy,low%20morbidity%20and%20mortality%20rates.