duedenal diverticulitis lecture for medical

diverticula

1. Duodenal Diverticulum ” Grand Round ” Ahmed Alhamss Qutaiba Sulaiman Supervised by: Dr. Osama Abu Zaid

2. Case presentation 73 yrs old M pt MF, ,was completely well till 10 hours PTA when he started to c\o sudden onset periumbilical pain, dull ,not radiated, aggravated by food intake, relieved by vomiting ,8\10, associated with vomiting 2 X, small amount, food particles, 1 spike of feverish sensation, no other associated symptoms. Chronic Lt leg swelling !! Medication history: LASIX, ASPIRIN, acetaminophine .

3. Physical examination: V\S: T:37.8, RR:18 BP:141/70, PO2:95% WT:104 KG. P :70, normal volume &character Patient looks well, CAO , lying on bed in pain in mild distress, no pallor ,no cyanosis, no jaundice.

4. Chest :GAEVB, No added sounds CVS : Nomral S1 and S2,no added sounds. Abdomen : Symmertical , distended with fat, no scars, no dilated veins,periumblical & epigastric tenderness, no guarding, no rigidity. I ntact hernial orifices.+ve bowel sounds. DRE : no melena , no hematochezia , no palpable masses LEFT LEG SWEELING NOTICED.

5. Diagnostic workup WBC:15.9/ 96 , HB :16.2/47 , PLAT: 263. CRP : 43 RBS:179 BUN:47 , Cr: 1.4 ,Na: 145 , K: 4.1

6. Imaging ABDOMEN XRAY: Distended stomach, with no signs of small or large bowel obstruction. Chest x ray: normal no air under diaphragm.

7. Management plan Pt kept on strict NPO. IVF 150 ml\hr G.S 0.45%. Strict input\output NGT ABD-PELVIS CT SCAN with IV& ORAL CONTRAST. CARDIOLGY COSULT IDs CONSULT. Meronem , perfalgan,Nexium,Clexan started .

8. LABS ON 2ND DAY: WBC:22/90,LIPASE:1278 , AMYLASE :712, CRP:231 CT scan was done: No evidence of Acute pancreatitis

9. LABS ON 4TH DAY:CRP:99,WBC:6.7, K:4.34, ( CFD INTIATED) LABS ON 5TH DAY:CRP:52 ,( FFD INTIATED ) 6 TH DAY OF ADMISSON PATIENT WAS DISCHRGED ON ARGIMENT,DIFLUCAN,CIPRO,CURAM .

10. Literature Review Outlines : Introduction Clinical presentation Diagnosis Management

11. Introduction The duodenum follows the colon as the 2nd most common place for diverticula. It has been identified in only 5–10% of patients undergoing radiological or endoscopic procedures for other etiologies and in 15–23% at times of autopsy.  Duodenal diverticula are rare in patients younger than 40 years .

12. Types : Primary congenital diverticula: ( extremely rare, Intraluminal, also known as windsock diverticula, they are due to incomplete recanalization of the duodenum and are composed of all layers of the intestinal wall. ) 40 % of cases having intraluminal diverticula are associated with other congenital malformations

13. Acquired pseudodiverticula : Extraluminal pulsion diverticula which consist of mucosal or submucosal outpouchings herniated through a muscle defect in the bowel wall  at sites where the muscularis layer is weakened by the passage of blood vessels . Represent more than 90% of duodenal diverticulae

14. U sually occur within the 2 ND portion of the duodenum ( 60%) and less commonly in the 3 RD (30%) and 4 TH (8%) portions . R arely occur in the first part of the duodenum(< 1 %). When they occur in the 2nd portion, most (90%) are noted on the medial wall around the ampulla ( i.e.periampullary / perivaterian ), 8% are seen posteriorly, and 4% occur on the lateral wall . Multiple diverticula present in 10–15% of patients.

15. Clinical presentation Duodenal diverticula produce symptoms in 5% to 10% of cases

16. Biliopancreatic manifestations : These are the most common. Cholidocholithiasis ” pigmented stones” which may result in obstructing jaundice and cholangitis Mechanical obstruction of the common bile duct (CBD) by the diverticulum itself ( Lemmel's syndrome ) Acute pancreatitis if the pancreatic duct has been obstructed.

17. Diverticulitis Compared with their colonic counterparts, duodenal diverticula are less common sites of inflammation because of : larger size, more rapid intraluminal flow, and smaller bacterial count.

18. Diverticulum perforation : Less than 200 cases of perforated duodenal diverticulum have reported. It’s the least common complication but the most serious one which requires prompt treatment because of its high mortality rate 30%.

19. Most of these perforations (78%) are seen within the second portion of the duodenum, mainly along the medial wall, within 2 cm from the ampulla of v ater . The most common cause was diverticulitis, seen in 62% of patients, followed by enterolithiasis (10%), iatrogenic (5%), ulceration (5%), trauma (4%), and foreign body (2 %).

20. clinical presentation The clinical presentation varies greatly and requires a high index of suspicion . As most perforations are retroperitoneal, symptoms are usually nonspecific including RUQ pain associated with nausea and vomiting, and rarely include peritoneal irritation Retroperitoneal contamination leads to retroperitoneal abscess formation and sepsis .

21. O ften mistaken for other intra-abdominal processes such as cholecystitis, pancreatitis, peptic ulcer disease, colitis, or retrocecal appendicitis.

22. The most challenging differential diagnoses is perforated duodenal ulcer. A distinguishing feature is the location of perforation. ( most ulcers involve the duodenal bulb, whereas diverticula affect more distal portions)

23. Diagnosis: Ultrasound studies are rarely informative Although difficult to elucidate on imaging, the most sensitive exam to detect a duodenal diverticulum perforation is an abdominal CT scan, which can reveal: T hickened bowel wall, mesenteric fat stranding, and an extra luminal, retroperitoneal collection of air or fluid.

24. Management Due to the rareness of perforated duodenal diverticulum, surgical treatment guidelines are lacking .

25. Surgical intervention has always been the mainstay for symptomatic/complicated duodenal diverticula W ith advancement of imaging, medical treatment, and proper intensive observation, and high rate of morbidity postop, including duodenal leak and fistulization , The option of conservative treatment has become more and more implicated.

26. Conservative approach In mildly affected with no evidence of impending sepsis . In a patient of advanced age or with multiple medical comorbidities, provided symptoms are mild and there is no evidence of impending sepsis.

27. “Taylor's approach for upper GI perforation” I ncludes bowel rest with or without nasogastric tube suction, intravenous hydration and antibiotics, total parenteral nutrition, and when needed, percutaneous catheter drainage of retroperitoneal collections. Close clinical observation is mandatory and surgical intervention is indicated if conservative management fails.

28. It may be advisable to perform radiographic studies with water-soluble contrast between the fifth and seventh day, before starting oral alimentation with fluids.

29. Surgical treatment:   Diverticulectomy with single or double-layer closure is the most frequent reported alternative if inflammation permits. Some cases of simple intra-abdominal drainage were also successful.

30. When substantial duodenal or retroperitoneal inflammation is present: The perforated diverticulum should be excised and the duodenum closed with a serosal patch from a jejunal loop. If the surrounding inflammation is severe, it may be necessary to divert the enteric flow away from the site of the perforation with a gastrojejunostomy or duodenojejunostomy . Interruption of duodenal continuity proximal to the perforated diverticulum may be accomplished by pyloric closure with suture or a row of staples

31. T he complications of the surgical interventions applied include: D uodenal fistula intraabdominal abscess Sepsis Pancreatitis.

32. All intraluminal duodenal diverticula require treatment as recurrence of symptoms is certain . Curative treatment consists of removal of the intraluminal diverticulum by laparotomy and duodenotomy or by endoscopic resection. E ndoscopic approach in the setting of massive hemorrhage or perforation with intra-abdominal contamination secondary to intestinal contents is discouraged.

33. Any question