The Early Diagnosis of the Acute Abdomen by Sir Zachary Cope

A classic I've heard. Will summarize each chapter here to help me remember the key points.

1. The Principles of Diagnosis

Need to make a diagnosis because an "acute abdomen" = "surgical abdomen" and often requires surgery. Making the diagnosis early is often advantageous. 

Localization of inflammatory lesions is aided by knowledge of anatomy (think referred pain, innervations, rigidity in proportion to somatic innervation, etc)

Localization of obstructive lesions is aided by knowledge of physiology. Distension causes pain. Pain is mid-line until peritoneal nerves are directly irritated.

Exogenous steroids can diminish inflammation and thus mask early signs of peritonitis.

2. Method of Diagnosis: the history

Have a routine

I. chronology (time and mode of onset(acute vs. insidious))

II. pain (onset, distribution, and the seven characteristics)

III. anorexia is usually very significant

IV. nausea

V. vomiting is due to irritation of peritoneum or mesentary OR obstruction of an involuntary muscular tube. In obstructions, the onset of vomiting relative to pain can help localize proximity of the blockage. Is there bile in the vomit? Feculent vomit is pathognomonic of distal jejunal obstruction.

VI. bowels can be constipated, diarrhea common sign of appendicitis in children. Watery diarrhea with partial small bowel obstruction.. Blood or mucus in the rectum is suspicious for intussusception.

VII. menstruation history to rule out ectopic pregnancy

VIII. previous illness

3. Method of Diagnosis: the examination of the patient

I. general appearance: watch the patient quietly, observe the attitude in bed (restlessness from colic vs. immobility in peritonitis)

II. pulse: changes only in late disease

IIa. BP: drops late in shock

III. respiration rate: goes up late in abdominal disease, early if thoracic disease.

IIIa. chest: 

IV. temperature: high fever is unusual during early stages of abdominal disease except for severe pancreatitis.

V. abdomen: inspect, movement on respiration, palpation, percussion. Rigidity can be absent in the elderly. Hyperesthesia is not a useful diagnostic sign.

VI. Iliopsoas test

VII. liver: percussion can expose free peritoneal air if dullness is missing

VIII. rectal exam: test for tenderness against pelvic peritoneum. Don't forget to use stoma if patient has one.

IX. thigh rotation test

X. spine: 

4. Method of Diagnosis: the grouping of symptoms and signs

I. Abdominal pain by itself

II. Central abdominal pain: examine the patient again in 2-3 hours (don't forget about glaucoma)

III. Severe central pain with shock: acute pancreatitis, ruptured aortic aneurysm, dissecting aneurysm, mesenteric thrombosis, splenic rupture, ectopic pregnancy rupture.

IV. Pain with vomiting and increasing distention but no rigidity: intestinal obstruction

V. Abdominal pain with constipation, increasing distention, and little or know vomiting: large bowel obstruction, uremia, lead poisoning. In infants remember pneumococcal peritonitis, intussusception (barium enema).

VI. Severe abdominal pain with collapse and general rigidity of the abdominal wall: visceral perforation, 

- RUQ pain and rigidity: acute cholecystitis, leaking duodenal ulcer, amebic hepatitis

- LUQ pain and rigidity: acute pancreatitis, perforated gastric ulcer, inflamed jejunal diverticulum, splenic artery aneurysm, splenic rupture, and leukemia?

- RLQ pain, tenderness, and rigidity: acute appendicitis, pancreatitis, gallbladder, duodenum, kidney, ileocecal lymph nodes, meckels diverticulum, lileitis, retained testis, fallopian tube, ovary (chapter 7).

- LLQ pain, tenderness, and sometimes rigidity: diverticulitis of the left colon, crohns, acute pyelitis, left pleurisy.

- Hypogastric pain and rigidity: perforated inflamed appendix, perforated sigmoid diverticulum, uterus, fallopian tubes, ovaries

5. Laboratory and Radiological Tests

CT is the imaging of choice for

1. appendicitis
2. perforation
3. pancreatitis
4. diverticulitis
5. abscess
6. aortic aneurysm and rupture
7. renal colic

HIDA for cholecystitis after ultrasound

Ultrasound for

1. aortic aneurysm
2. fuptured ovarian follicle
3. ectopic pregnancy
4. tubo-ovarian abscess

Plain X-ray or X-ray with contrast for

1. perforation
2. intestinal obstruction
3. intestinal inflammation

6. Appendicitis

Often significant inflammation before symptoms are noticed.

Appendix can be in different locations leading to different presentations.

• ascending
• iliac (appendix above the brim of the true pelvis)
• pelvic (appendix below the brim of the true pelvis) has less rigidity if any upon perforation and the pain stays epigastric for longer.
• retrocecal is when pain is felt later and often starts localized

History

Indigestion, gastritis, flatulence.

Irregular bowel movement.

Signs and Symptoms

1. Pain often referred at first to epigastric or umbilical region, sometimes more like tenesmus.
2. Anorexia, nausea, and vomiting a few hours after initial pain. If patient is hungry, doubt the diagnosis of acute appendicitis.
3. Local tenderness comes late, try percussion and DRE.
4. Hyperesthesia is inconstant
5. Rigidity of abdominal muscles over inflamed area. Watch to see if moves with respiration. Pelvic appendix will not cause rigidity.
6. Fever develops before 24 hrs have passed. 
7. Constipation and/or diarrhea.
8. Pulse acceleration corresponds to peritonitis or 
9. Distention of the cecum can be present due to adynamic ileus. 
10. Testicular symptoms 

Order of Occurrence of the Symptoms

1. Pain
2. anorexia, nausea, or vomiting
3. tenderness
4. fever
5. leukocytosis

Diagnosis after perforation is due to accentuated pain and renewed vomiting. 

7. The Differential Diagnosis of Appendicitis

The pain part

• Influenza
• Diaphragmatic pleurisy
• Spinal disease
• Typhoid fever
• Acute porphyria
• Gastroenteritis
• Infectious hepatitis
• Diabetes with DKA

The peritonitis part

• Intestinal obstruction
• thrmbosis or embolism of mesenteric vessels
• acute pancreatitis
• pneumococcal peritonitis
• Pyelitis
• general peritonitis (from ruptured ulcers)

Things that mimic a perforating or perforated ascending appendix

• cholecystitis
• inflamed duodenal ulcer
• pyelonephritis
• hydronephrosis
• pyonephrosis
• kidney/ureter stone
• perinephric disease
• omental torsion

Differential of inflamed iliac appendix (this one should be easiest)

• perforated duodenal ulcer (look for free air because free air is almost never present in acute appendicitis
• Crohn disease
• Carcinoma
• Ureteral stone
• Meckel diverticulum
• Ruptured or bruised right rectus muscle
• cecal ulcer

Differential diagnosis for pelvic appendix.

A) Male

• large bowel obstruction
• ileal obstruction
• diverticulitis
• typoid ulcer perforation
• stone in ureter
• gastroenteritis
• pelvic abscess

B) Female

• Dysmenorrhea
• ectopic pregnancy
• twisted pedicle, rupture of ovarian cyst, torsion of ovary
• inflamed fibroid
• hydrosalpinx
• salpingitis or pyosalpinx
• endometrioma rupture

8. Diverticulitis 

Pathogenesis

Fecolith obstructs lumen, usually in sigmoid

Symptoms

hypogastric pain

anorexia, nausea, vomiting

shift of pain and tenderness to left iliac fossa

diarrhea

fever and leukocytosis

mass in left iliac fossa

Secondary intestinal obstruction

can happen from acute diverticulitis

usually small bowel

9. Perforation of a gastric or duodenal ulcer

Early, intermediate, and late stages of symptoms

things get better around 12 hours into the pain, don't fall into the trap!

Differential diagnosis

• severe colic (biliary or renal)
• pneumonia or pulmonary infarction
• gastric crises of tabes dorsalis
• acute pancreatitis
• acute perforative appendicitis
• acute intestinal obstruction
• ruptured ectopic pregnancy
• dissecting thoracic or ruptured abdominal aortic aneurysm
• general or diffuse peritonitis
• postemetic rupture of esophagus
• mesenteric embolus or thrombosis

10. Acute Pancreatitis

Etiology

EtOH

Gallstones

trauma

hyperlipidemia

hyperparathyroidism --> hypercalcemia

thiazide diuretics

Signs and symptoms

• Pain
• vomiting or retching
• fever
• Tenderness
• rigidity is not constant

Signs from pancreatic edema

palpable

jaundice

obstructive vomiting

Signs from extravasation of blood

ecchymosis (Turner sign and Cullen sign)

Labs

hyperglycemia

glycosuria

amylase

hyperlipidemia

albuminuria

11. Cholecystitis and other causes of acute pain in the RUQ

Usually...

• cholecystitis

steady pain, subsides over 4-6hrs, 

chronic hydrops of gallbladder may form after impaction of stone in duct

jaundice may be transient if stone passes

Signs and Symptoms

Pain often midline, unrelenting constant, 

Anorexia/nausea/vomiting

Jaundice

Fever, very high temps likely to be cholangitis

Palpable gallbladder

Tenderness and rigidity

Acalculous cholecystitis is most often observed when patient is one TPN

• biliary "colic"

• duodenal ulcer

Pain comes 2.5 hrs after meals

Retroperitoneal perforation mimics renal problems, because there can be increased micturition and even hematuria. Also CVA tenderness.

• hepatitis

Tenderness all over the liver, including the lateral aspect.

but must rule out...

• appendicitis
• renal pain or colic
• MI and angina pectoris

EKG

Tropins

• pleurisy or pneumonia

high fever

initial rigor

pain on top of right shoulder

hemoptysis

12. Acute abdominal lesions in left hypochondrium

fundus of stomach

- rare to have perforated ulcer in the fundus

spleen

- rupture, think sickle cell, may be friction rub

- splenic artery aneurysm, watch for in pregnant women, 

pancreas tail

- acute pancreatitis

splenic flexure of colon

- carcinoma

- stricture

- diverticulitis

upper pole of left kidney

- perinephric abcess more dangerous on left side because inflammation can go up to diaphragm. Irregular fever, 

Aorta

- aneurysm

Jejunum

- jejunal diverticulitis, watch for flatulence, borborygmi, and diarrhea. 

13. The Colics

Tubes that we have to consider contracting against resistance are:

- Stomach

- Small bowel from entereitis or obstruction OR lead poisoning. Epigastric region, vomiting

- Cystic, hepatic, and common bile ducts (rule out acute porphyria)

- Gallbladder

- Pancreatic duct (duct of Wirsung)

- Colon refers to hypogastrium, constipation, colitis, sysentery, stricture

- Ureters, pain can refer to testicle/vulva, check for phyeresthesia, vomiting frequent, 

- Uterus, dysmenorrhea

- Fallopian tubes

They all have spasmodic pain, associated with sympathetic NS symptoms (pallor, weak pulse, vomiting, low temp). Restless patients don't want to remain still. 

14. Acute Intestinal Obstruction

a) strangulated hernia

b) adhesions

c) intussusceptions

     C1) ileocecal inussusception in kids

d) cancer

e) volvulus

     e1) volvulus of stomach is rare, elderly people, vomiting and then continued retching, no bile comes out, steady pain, associated with paraesophageal hiatal dephragmatic hernia.

f) pyloric stenosis (kids)

g) atresias and annular pancreas (kids)

Symptoms

Pain

Vomiting occurs sooner the higher up the obstruction, colonic obstruction may only result in nausea and anorexia

Constipation not always evident at first. Diarrhea is very common in partial obstruction. Flatulence is rare in both.

Distention occurs very late, more distal = more distended.

Tenderness after distention.

Rigidity is unusual.

Peristalsis visible in skinny patients.

Borborygmi can rule in, but its absence cannot rule out.

Shock late, you missed the diagnosis.

Differential includes:

- (distention absent) renal colic, biliary colic, gastric crisis.

- (distention present) uremia, mesenteric thrombosis/embolism, peritonitis.

Diagnose with:

- plain films vertical and decubitus

Colonic obstruction presents differently depending on competence of ileocecal valve. If incompetent, then looks similar to SBO on radiography.

70% colon cancer. Early symptoms include diarrhea, blood, mucus.

Then later constipation that gradually increases.

10% volvulus possible at ileocecal region and sigmoid region.

5% diverticulitis

?% fecal impaction

Differential includes:

- colitis with distention (toxic megacolon)

- uremia

- peritonitis

- reflex paralysis of colon vs adynamic ileus (opioids) vs colonic ileus

15. Intussusception and other causes of obstruction

16. The early diagnosis of stragulated and obstructed hernias

17. Acute abdominal symptoms due to vascular pathology

18. Acute abdominal symptoms in women

19. Early ectopic gestation

20. Acute abdominal disease with genitourinary symptoms

21. The diagnosis of acute peritonitis

22. The early diagnosis of abdominal injuries

23. The postoperative abdomen

24. The acute abdomen in the tropics

25. Diseases that may simulate the acute abdomen

26. Acute abdominal pain in the immunocompromised patient

27. Abdominal catastrophes when sensation is impaired

Didn't have time to take notes on these last chapters as medicine starts tomorrow morning and it's time to go to bed. Was a bit rushed because this book is due back at the library tomorrow.

Nephrology Elective

Again, a sample of some articles I read, and some commentary on some things I learned.

Venous and Arterial Thrombosis in Dialysis Patients by Ocak et all, 2011

Dialysis patients have clearly elevated risks of venous thrombosis AND arterial thrombosis.

Prevalence of thrombophilic mutations in patients with unprovoked thrmboembolic disease. A comparative analysis regarding arterial and venous disease by Mandal E et all, Hippokratia 2012, 16, 3: 250-255.

Concluded that primary thrombophilic states (mutations) lead to not only venous thrombotic events but also arterial thrombotic events.

Then two great articles on preeclampsia of all things. I did a presentation on this during my first week and actually found it to be quite interesting. 

I've decided to keep the articles that I read for professional learning in refworks folders, and use this blog just to keep track of the books that I read. Refworks is a bit more searchable and links directly to my university library that subscribes to the medical journals so that I can get PDF texts when I need them. 

Next up, basic science, then I start medicine at Highland.

GI Consult Elective

I'll summarize some of the things I read for this elective below. 

Otherwise, I spent my days doing new consults and following up on my old consults. I learned a whole bunch and became clearer in my head that I'm not really drawn toward the procedural side of medicine. GI specialists know a lot of medicine but they are also technically adept at using endoscopes and all the tools that you can put on those scopes these days.

"Long-Term Colorectal-Cancer Incidence and Mortality after Lower Endoscopy" by Reiko Nishihara et all, NEJM 9/19/13

Colonoscopy and sigmoidoscopy are associated with a reduced incidence in left sided distal colon cancer. Right sided or proximal colon cancer is not reduced as much by colonoscopy, a fact that we learned last year. The polyps and other precancerous lesions are much more difficult to see in the right colon due to a different genetic mutation pathway. Cancers that pop up between colonoscopies are likely to have the "serrated pathway" mutations.

"American College of Gastroenterology Guideline: Management of Acute Pancreatitis" by Scott Tenner et all, 7/30/13

- Mild Acute Pancreatitis is self-limiting, does not have organ failure and/or pancreatic necrosis. Patients start eating again within 48hrs.

- Moderately Severe Acute Pancreatitis has local complications (fluid/necrosis) and/or transient organ failure (<48hrs).

- Severe Acute Pancreatitis has two phases:

1. early (first week) has SIRS and/or organ failure.
2. late (after the first week) characterized by local complications (peripancreatic fluid/necrosis/pseudocysts)

Diagnosis

1. Two of three criteria

     i) abdominal pain (epigastric or LUQ, constant, radiates to back, chest, or flanks)

     ii) serum amylase (rises in hours, falls in days) and/or lipase (more specific, stays elevated longer)greater than 3X the upper limit of normal

     iii) characteristic findings from abdominal imaging

2. CT and MRI should be reserved for patients who fail to improve clinically within the first 48-72hrs after hospital admission.

Etiology

1. Ultrasound on everybody to rule out gallstones.

2. History of EtOH (need 5 years of heavy drinking? If no, check serum triglycerides.

3. In patients older than 40yo, tumor should be considered.

Initial Assessment and Risk Stratification

1. Assess hemodynamic status.

2. Assess risk (age, obesity, mental status, comorbidities, SIRS, Labs, imaging)

3. If signs of organ failure, admit to ICU

Initial Management

1. Aggressive hydration (250-500mL/hr) is most beneficial during the first 12-24hrs. LR might have some advantages because prevents the hyperchloremic non-anion gap metabolic acidosis that is possible with large volumes of normal saline.

ERCP

do it within 24hrs of admission if cholangitis is sure.

don't do it if there is no evidence of obstruction

MRCP if no jaundice or cholangitis

use stents and NSAID suppositories after ERCP

Antibiotics

Give for extrapancreatic infection.

No role for prophylactic antibiotics

Carbapenems, punolones, and metronidazole penetrate pancreatic necrosis.

Nutrition

Start oral feeding asap when nausea and vomiting resove

Enteral nutrition better than parenteral if PO route not available.

Surgery

cholecystectomy before discharge unless necrotizing in whic case wait until inflammation subsides.

Persistence of Nondysplastic Barrett's Esophagus Identifies Patients at Lower Risk for Esophageal Adenocarcinoma: Results from a Large Multicenter Cohort by Srinivas Gaddam et all

Cyclic Vomiting Syndrome and Abdominal Migraine in Adults and Children by Randolph W. Evans and Chad Whyte

CVS is 5 separate attacks, episodic, stereotypical, vomiting, symptom free between attacks, not attributable to another disorder.

Epidemiology

2% of children

headache/migraine history

slight male predominance

Clinical Features

Four phases to each episode:

1. well phase without symptoms
2. prodrome with pallor, sweating, and nausea
3. intense vomiting
4. recovery phase

Pathophysiology

similar to migraines, periaquaductal grey matter, autonomic dysfunction.

"brain-gut" disorder mediated by the neuroendocrine system as evidenced by ACTH, ADH, cortisol, and other endocrine substances that rise in serum. CRF is stimulated by stress in the hypothalamus and it leads to delayed gastric emptying due to inhibiting the dorsal motor nucleus of the vagus nerve. TCAs inhibit the promoter activity of the CRF gene, and thus efficacious in treating CVS.

Differential Diagnosis

acute illness causes of nausea and vomiting.

Treatment

Supportive measures (hydration, electrolytes, quiet, dark, ondansetron, benzodiazepines, diphenhydramine.

Sumatriptin can be taken upon onset of episode.

Abortive agents include NSAIDS (ketorolac) and opioids.

Treatment with amitriptyline, venlafaxine

Prognosis

CVS resolves in many children by teenage years. 86% of adults are cured with TCAs.

abdominal migraines 

Epidemiology

slight femal predominance

5-15 years old

Clinical Features

Recurrent , episodic attacks of abdominal pain with associated nausea, vomiting, and or lethargy lasting as long as migraines.

Periumbilical pain.

Often premonition.

Pathophysiology

unknown

Differential Diagnosis

other causes of abdominal pain

Treatment

treated with prochlorperazine and eletriptan

avoid triggers, dietary management

IV valproate

Pizotifen, flunarizine

Propanolol, cyproheptadine.

I also read a whole bunch of textbook chapters from MD Consult, and learned a lot about diarrhea. I am starting to realize that information technology has changed medicine more quickly than the training can keep up with. As a medical student, I am able to become an expert on tiny pieces of medicine relatively quickly in a way that would not have been possible 10 years ago. It makes me think that the fragmentation of care is not really necessary. Why can't a family doctor refer a complicated patient to herself and spend the 3 or 4 hours that are required to access the detailed information about the complex management necessary. That same 3-4 hours will be spent by a slew of specialists who will use the very same resources (or likely have memorized them) to come up with the same answer. It seems to me that family doctors should have yearly exams, rotating through all of the traditional specialties each year, open book, to ensure that they are on top of their game, because they must recognize and diagnose diseases of every organ system. Better yet, patients should start out at specialists (knee pain, go to an orthopedic specialist) and then get referred to family doctors for management of complex, multiorgan/biopsychosocial challenges. Pay scales should be revered accordingly because specialists will actually need much less training than generalists. Training for specialties can be substantially shortened by skipping all the generalized stuff at the beginning. Technical wizardry would be mastered much more quickly just out of high school so why not get those same folks before they "waste their time" learning how to talk about feelings with their patients.