acute abdominal infections presentation 1209102520194201 9

8/3/2019 Acute Abdominal Infections Presentation 1209102520194201 9

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Acute Abdominal

Infections

Ana Corona, FNP-StudentUniversity of Phoenix

2002

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Acute Abdominal Infections

Abdominal infections can be minor or lifethreatening.

70% of diagnoses can be made based on

history alone.

90% of diagnoses can be made based on

history and physical exam. Expensive tests often confirm what is

found during the history and physical.



The Abdominopelvic Cavity: 2

Portions

The Upper Abdominal

Portion:

The LowerPelvic Portion

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The Upper Abdominal Portion

Stomach

Liver

Spleen Pancreas

Gallbladder

Small intestine

Large intestine

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The Lower Pelvic Portion:

Rest of largeintestine

Rectum Urinary bladder

Internal

reproductiveorgans

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Clinical Subdivisions of the Abdomen

The abdominal cavity is

divided into 4 sectionsFour quadrants:

Right UpperQuadrant

Right LowerQuadrant

Left Upper Quadrant

Left Lower Quadrant

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Abdominal Regions

The abdomen can be further

subdivided into thefollowing regions:

Right hypochondriac region

Left hypochondriac region

Epigastric region

Right lumbar region

Left lumbar region

Umbilical region Right iliac (inguinal) region

Left iliac (inguinal) region

Hypogastric region

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Acute Abdominal Infections

Acute Abdominal pain is the main,

presenting symptom of patients with Acute Abdominal Infections

Abdominal pain can represent processes as varied as benign, self-limited viral gastroenteritisto a perforated hollow viscus that can be fatal without intervention

Epigastric pain and indigestion is consideredheart ischemia until proven otherwise in malesover 35 years, females over 45 years, and forpatients with a cardiac history.

Large majorities of females with lower

abdominal pain have gynecological problems.



Referred Pain

Perforated Ulcer

Biliary Colic

Renal Colic

Dysmenorrhea/Labor

Renal Colic (Groin)

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Referred Back Pain

Pain Location Visceral disease

T10-12 Peptic ulcers and tumors of thestomach, duodenum or pancreas

Low back pain Ulcerative colitis, diverticulitis, PID,

cancer of the ovary, uterus, or prostateCVA Renal disease

Thoracic-lumbar Aortic dissecting aneurysm

Note Back pain referred from visceral diseasereveals no stiffness and movement of the back does not increase the pain.



Abdominal Pain Locations Related to Possible Diagnoses

RUQ LUQ

Appendicitis

Biliary Colic Gallbladder disease Gallstones

Liver disease Kidney stones

MI/Ischemia Pancreatitis Peptic Ulcer Pneumonia Pulmonary Infarct

Subphrenic Abscess

Diverticulitis

Empyema

Gastric ulcers/Gastritis

Kidney stones

MI/Ischemia

Pulmonary embolus

Pericarditis Splenic rupture

Pancreatitis

Pneumonia




RLQ LLQ

Appendicitis

Crohn’s disease Cholecystitis Diverticulosis Ectopic Pregnancy Endometriosis Fecal perforation Gastroenteritis Hernia Intestinal obstruction

Ovarian cyst PID Ruptured Peptic Ulcer Ulcerative Colitis

Ureteral Stone

A ppendicitis (early)

Colon cancer/perforation Diverticulitis

Ectopic pregnancy

Endometriosis

Hernia

Intestinal Obstruction

Ovarian cyst

PID Sigmoid perforation

Ulcerative colitis

Ureteral stone




Epigastrium Diffuse

Cholecystitis Myocardial

Ischemia

MyocardialInfarction

Pancreatitis

Peptic Ulcer

Reflux Esophagitis

Appendicitis

Abdominal Aorta Aneurysm

Bacterial Peritonitis Colitis Gastroenteritis IBD Intestinal Ischemia

Intestinal Obstruction Pancreatitis Sickle Cell Crisis

Toxic Metabolic Etiology



Pain Associated with Acute Abdominal Infections

Dull Pain Dull pain is commonly associated with

inflammation and low-grade infection.

Intermittent Pain Intermittent pain is commonly associated with gastroenteritis and

small bowel obstruction.

Severe Pain Severe pain controlled by medication iscommonly associated with pancreatitis,

peritonitis, small bowel obstruction,renal colic, and biliary colic. Severepain not controlled by medications iscommonly associated with infarction

or rupture.

E i l Hi



Essential History

A carefully taken history describing the pain

is the most powerful diagnostic tool. The following features must be determined:

Onset: How did pain start? -

Acuteness: Sudden (minutes) - ruptured viscous,

aneurysm or ectopic pregnancy

over 1-2 hours - pancreatitis, bowelobstruction, renal colic

over several hours - cholecystitis,

appendicitis, PID



Essential History Continued: Nature of pain

When did it start? Duration:

>6 hours severe pain suspect significant illnessWhere did it start? Initial site:

Has it shifted? (e.g... Appendicitis)

Colic:Features

Severe pain, poorly localized, restlessness sweating,

reflex vomiting Caused by obstructed "tube" with a typical time

course

Bowel, Gall bladder, Ureter

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Nature of Acute Abdominal Pain

Inflammatory

Features:

Pain is Constant

Aggravated by movement or coughing Localized

Caused by inflamed organ:

Appendix Gallbladder

Colon



Further History: Associated Signs &

Symptoms Nausea/Vomiting

Follows onset of pain in surgical causesMay be: reflex (in colic), or from

obstructed bowel

Is often absent in gynecological causes Constipation

Diarrhea

1 or 2 loose stools common at onset of peritonitis

Profuse in gastroenteritis and

inflammatory bowel disease (IBD)



Further HistoryBlood in stool IBD, Intussusception, Ischemic bowelFever Mild in early appendicitis

If high consider abscess, pneumonia, systemic

illnessUrinary Symptoms Dysuria

Urethral "burning" during micturationUTI, Bladder Stone

Abdominal pain during micturationPelvic peritoneal irritation



Further History

Frequency

UTI, Stone in lower ureter

Hematuria

UTI, Stone, Tumor

Menstrual Symptoms alert you to GYN causes

LMP date

Menstrual irregularity Vaginal discharge- alert to GYN causes

C id R l E M l & V i l/R l



Consider Rectal Exam on Males & Vaginal/Rectal on

FemalesRectal Examination

Rectal mass - may cause large bowel obstruction Abdominal pain on palpating pelvic peritoneum- pelvic

peritonitis

Blood - IBD, ischemic bowel, hemorrhoids

Impacted stool- constipation

Vaginal Examination

Cervical pain - Pelvic inflammatory disease (PID), ectopic

pregnancy Purulent discharge - PID

Bulky uterus - pregnancy

Adnexal mass - ectopic pregnancy, ovarian cyst, tumor.

Cli i l D i i M ki A i i d M di l C



Clinical Decision Making: Anticipated Medical Care

of Acute Abdominal Infection

Lab Tests CBC with differential, electrolytes, BUN,

creatinine, glucose, LFTs, amylase,lipase, PT, PTT (WBC >20,000 suggestssepsis and may require surgery)

Radiology Tests Abdominal ultrasound, spiral CT (nooral contrast needed), abdominal CT(oral contrast needed), x-rays of thechest and abdomen, intravenous

pyelogramOther tests Pelvic/Rectal exam, orthostatic vital

signs, Stool Guiac/culture, Urinalysis

Diet NPO



Clinical Decision Making: Anticipated Medical Care

of Acute Abdominal Infection

Medications Anti-inflammatory, antipyretic, antiemetic,

Analgesic, Antibiotics

Implicationsfor Practice:

Disposition

The FNP must determine what is the mostappropriate setting for care. Whether to

initiate treatment as an outpatient setting, referpatient to the hospital or to call 911,depending on patient’s health status

Worse case

scenario

An unsuspected abdominal aortic aneurysm

rupture resulting in sudden circulatory collapse from loss of volume. An older adultmale with a history of DM, HTN, andsmoking is the most common patient type foran aneurysm.

Ri h U A Abd i l P i



Right Upper Acute Abdominal Pain:

Diagnostic Tools and Initial Management

Diagnostic Tools: Erect Chest X-ray

Ultrasound

Amylase, Creatinine, Urea, Electrolytes Full Blood Count

Urinalysis

ECG Liver Function Tests

Initial management will depend on specific

diagnosis

Epigastric and Left Upper Ac te Abdominal Pain



Epigastric and Left Upper Acute Abdominal Pain:Diagnostic Tools & Initial Management

Diagnostic Tools

Erect Chest X-ray

Erect and Supine Abdominal X-ray

Amylase, Creatinine, Urea, Electrolytes

Full Blood Count

Urinalysis ECG


diagnosis



Right Lower Acute Abdominal Pain: Diagnostic



Right Lower Acute Abdominal Pain: Diagnostic Tools & Initial Management

Diagnostic Tools:

Most of these diagnoses can be differentiatedclinically.

U/A - to exclude an unsuspected urinary cause.

Pregnancy test - in women of childbearing potential

Ultrasound - if gynecological cause is suspected

Full blood count - of limited diagnostic value


diagnosis



Lower and Left Lower Acute Abdominal Pain: Diagnostic

Tools & Initial ManagementDiagnostic Tools:

Most of these diagnoses can be differentiatedclinically.

U/A to exclude an unsuspected urinary cause.

Pregnancy test if appropriate Ultrasound if gynecological cause is suspected

Full blood count

Erect and supine abdominal X-rays CT scan if complication of diverticular disease is

suspected

Initial management will depend on specific DX



Acute Appendicitis Appendicitis is an

inflammation of the vermiform appendix.

All people aresusceptible, the most

common occurrencesis between ages 20 and30 years, although itmay develop at any age.

It is very rare beforethe second year and

after the fiftieth year

Acute Appendicitis: Etiology &

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Acute Appendicitis: Etiology &

Pathophysiology Obstruction of the lumen with stool, tumors or

foreign bodies with consequent bacterialinfection is the most common theory.

The obstructed lumen does not allow drainage of

the appendix and as mucosal secretion continues,intraluminal pressure increases.

The resultant increased pressure decreases

mucosal blood flow and the appendix becomeshypoxic.

The mucosa ulcerates promoting bacterialinvasion with further inflammation and edema



Acute Appendicitis: Presenting Signs & Symptoms Diffuse periumbilical

pain and anorexia early

Nausea and Vomiting

Low grade fever

Associated S/S

Diarrhea, Constipation

Tachycardia

Pain may be worse onmoving or coughing

Pain localizes to theRLQ as peritonitis

develops

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Acute Appendicitis: Physical Findings

A dull right lower quadrant pain with rebound at

McBurney’s Point (just inside the iliac crest) Rovsing’s Sign: is an increase in right lower

quadrant pain initiated by palpation of the left lower

quadrant. It is suggestive of acute appendicitis. Obturator Sign: flexion and lateral rotation of the

thigh causes hypogastric pain, a sign of pelvic

abscess and appendicitis. Psoas Sign (iliopsoas test): extension and elevation

of the right leg cause pain, a sign of appendicitis.



Acute Appendicitis: Clinical

Decision Making

Essentially clinical

Rule Out urinary cause by urinalysis

Moderate elevated WBC (rarely >20,000cells/mm3)

Ultrasound in selected cases

X-rays and other tests are often negative



Acute Appendicitis: Differential Diagnosis

Abdominal Aorta

Aneurysm Colitis

Crohn’s disease

Diverticulosis Ectopic pregnancy

Fecal perforation

Gastroenteritis Hernia

Inflammatory Bowel

Disease

Intestinal Obstruction

Ovarian Cyst

PID

Pancreatitis

Sickle Cell Crisis

Spontaneous BacterialPeritonitis

Toxic MetabolicEtiology

Ureteral Stone

A A di i i T



Acute Appendicitis Treatment The main goal is diagnosis and immediate

hospital referral for surgical removal beforerupture.

NPO Intravenous fluids

Pain relief If hx < 48 hours early appendectomy with

antibiotics is recommended If history > 48 hours and mass palpable

NPO, IV fluids and antibiotics If abscess on Ultrasound - drainage Interval appendectomy after 6 weeks

A t Ch l titi



Acute Cholecystitis Is an acute inflammation

of a distendedgallbladder usually caused by an impactedstone in the cystic duct.

Stones may consist of cholesterol or pigmentssuch as Ca+ birubinate.

In the USA, over 80% of the stones arecholesterol.

Middle aged overweight

women

Ch l titi Eti l d

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Cholecystitis: Etiology and

Pathophysiology

Obstruction causes thegallbladder to becomedistended and inflamed.

Pressure against thedistended wall of thegallbladder decreases

blood flow Ischemia, necrosis, and

perforation of thegallbladder are possible

Acute Cholecystitis: Presenting Signs &

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Acute Cholecystitis: Presenting Signs &

Symptoms

Localized ordiffuse RUQ pain

Radiation to rightscapula

Vomiting and

constipation Low grade fever

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Acute Cholecystitis: Associated Signs &

Symptoms

RUQ pain may radiate to right scapula

Gastric pain

Pain may occur 30 to 90 minutes after afatty meal and lasts for several hours.

Jaundice is a sign of common bile duct

obstruction.

Acute Cholecystitis: Clinical Decision



Acute Cholecystitis: Clinical Decision

Making

Test findings: Elevated WBC, Serum bilirubin, Alkaline

phosphatase, and SGOT

Ultrasound

Diagnosis

Ultrasound shows gallstones and edematous wall



Acute Cholecystitis: Physical Findings Moderate fever

Patient lies still Tenderness and rebound RUQ ± tender mass

(+) Murphy's Sign (arrest of inspiration while

palpating over gall bladder) Kehr’s sign is pain referred from the epigastrium to

the right shoulder, a phenomenon associated with

biliary colic or acute cholecystitis. Kehr’s sign can also be from a diaphragm that is

irritated by blood in the peritoneum and often seen

with a ruptured spleen.

A Ch l i i Diff i l



Acute Cholecystitis: Differential

Diagnosis

Appendicitis Biliary Colic

Gallbladder disease Gallstones

Liver disease Kidney stones MI Diarrhea

Sensation of constipation

Tachycardia

Pain may be worseon moving orcoughing

Pain localizes tothe RLQ asperitonitis develops

A t Ch l titi T t t & M t



Acute Cholecystitis: Treatment & Management

Hospital Referral

NPO Bowel Rest

Nasogastric Suction Intravenous fluids Pain relief Antibiotics Surgery Referral on the first available elective list

Occasionally necrosis or perforation of gallbladder - urgent surgery

Surgery is indicated if the patient has symptoms. Symptoms resolve in 75% of patients



Acute Diverticulitis

Is an inflammation or

infection of herniations or saclikeprotrusions of the

mucosal wall at pointsof nutrient artery penetration

Incidence of diverticular diseaseincreases with age,>50% if age > 80 yrs

Acute Diverticulitis: Etiology &

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Acute Diverticulitis: Etiology &

Pathophysiology

It commonly occurs in the sigmoid colon. Cause of diverticulitis has been attributed

to a low-fiber diet and intraluminal

pressure. The resulting increased intraluminal

pressure causes the diverticulum to

perforate.

Bacterial spillage may occur with abscess

formation or frank fecal peritonitis.

Acute Diverticulitis: Signs & Symptoms



Acute Diverticulitis: Signs & Symptoms

LLQ pain relieved by defecation

Constant, severe left iliac fossa pain, Fever ± chills Colon tenderness, Bloody stools, intermittent

attacks

Associate Signs & Symptoms Diarrhea or Constipation & Flatulence

Acute attack closely resembles the symptom of

appendicitis except that the pain is in the left sideof the abdomen

Systemic evidence of sepsis with Hemodynamic

compromise and Mental status deterioration



Acute Diverticulitis: Physical Findings

Localized left iliac fossa guarding +rebound tenderness (generalized if freeperforation)

Palpable mass due to abscess Rectal Tenderness

Abdominal Distention



Acute Diverticulitis: Differential

Diagnosis

A ppendicitis (early)

Colon

cancer/perforation Diverticulitis

Ectopic pregnancy

Endometriosis

Hernia

IntestinalObstruction

Ovarian cyst PID

Sigmoid

perforation

Ulcerative colitis

Ureteral stone



Acute Diverticulitis: Clinical Decision

Making

Diagnosis

Clinically suspected

CT scan of the abdomen with oral contrastto identify complications

Leukocytosis

Acute Diverticulitis: Treatment &



Acute Diverticulitis: Treatment &

Management

Management:

NPO status

IV Normal Saline for fluid resuscitation Antibiotics

Hospital Referral/admission for surgical

resection

Acute Hepatitis



Acute Hepatitis

Acute hepatitis is an

infection of the livercaused by a Hepato-tropic virus (A, B, C, D,

E) and other viruses >250,000 new

infections occurannually in the USA.

Acute Hepatitis isencountered often inthe office and clinic.

Acute Hepatitis: Etiology & Pathophysiology

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Acute Hepatitis: Etiology & Pathophysiology

Hepatitis A – Fecal to oral transmission

Hepatitis B – Percutaneous (needle stick), sexual,perinatal transmission

Hepatitis C – Percutaneous transmission (IV drug

use accounts for over 50% of the reported cases.) Hepatitis D – IV transmission (IV drug users and

transfusions) Endemic among HBV (hepatitis B

virus) carriers in the Mediterranean bases and areasof South America

Hepatitis E – Waterborne transmission (epidemic inIndia, Africa, and Mexico)

Acute Hepatitis: Signs & Symptoms



Acute Hepatitis: Signs & Symptoms

RUQ Pain, Nausea & Vomiting, Diarrhea

Malaise, Low-grade Fever, Dark Urine Jaundice

Associated Signs & Symptoms

Clay-colored stools Influenza like symptoms

Joint pain

Urticaria Maculopapular rashes

Hematuria

Edema

Hepatitis B

Acute Hepatitis: Physical Findings



Acute Hepatitis: Physical Findings

Tender liver

Mild Hepatic enlargement Spleen may be enlarged

Jaundice may be present (maximal during 2nd week

of onset, then disappears during the next 2 - 8 wks)

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Acute Hepatitis: Differential Diagnosis

Appendicitis Biliary Colic

Gallbladder disease Gallstones Liver disease Kidney stones MI Myocardial

Ischemia

Pancreatitis

Peptic Ulcer

Pneumonia Pulmonary Infarct

Subphrenic

Abscess

Acute Hepatitis: Clinical Decision Making



Acute Hepatitis: Clinical Decision Making During Prodrome Phase:

Leukocyte counts may be normal or low normal

Atypical lymphocytes may be seen Elevated Serum Aminotransferase

ALT levels higher than AST

Serum Bilirubin peak (2nd week of acute illness) Vary between 5-20 mg/dl

Serum alkaline phosphatase levels normal or mildly

increased Serum albumin usually normal or slightly decreased

Serum globulins may mildly elevated

Prothrombin time is normal or minimally prolonged

Serology Diagnostics of Viral Hepatitis



gy g p

Agent: Acute Phase: Convalescence:

HAV Presence of IgM anti-HAV Development of IgG anti-HAV

HEV Presence of IgM anti-HEV Loss of HEV RNA; develop-

and/or HEV RNA ment of IgG anti-HEV

HBV Presence of HBsAg and/or IgM Loss of HBsAg: developmentof

anti-HBc anti-HBs and IgG anti-HBc

HDV Presence of HDV RNA or Loss of HDV RNA or antigen;

HDV antigen or IgM anti- development of IgG anti-

HDV in HBsAg-positive HDV or loss of anti-HDV patient

HCV Presence of development of Loss of HCV RNA

anti-HCV, presence of HCV

RNA

Acute Hepatitis: Treatment/Management & Outcome



p g

Management:: Symptomatic treatment, fluidresuscitation with normal saline, and referral for

hospital admission or outpatient follow-up care. OUTCOME:

Hepatitis A – Recovery within 6 to 12 months with

occasional relapses Hepatitis B – Recovery in > 90% of the cases

Hepatitis C – Incubation period 7 to 8 weeks,

course clinically mild, > 50% likelihood of chronicity, leading to cirrhosis in 20% of the cases

Hepatitis D – Progresses to chronic hepatitis

Hepatitis E – May need a liver transplant

Acute Pancreatitis



Acute Pancreatitis

Is an inflamed condition of

the pancreas that can beacute or chronic.

The most common cause of pancreatitis is alcohol intake.

The 2nd most commoncause is cholelithiasis.

A perforated duodenal ulcer

that erodes through thepancreatic wall and into thepancreas can progress topancreatitis.

Ac te Pancreatitis: Signs & S mptoms

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Acute Pancreatitis: Signs & Symptoms

May include sudden, intense, steady, boring pain in the epigastrium radiating to the

back, often increasing in the supine

position.

Associated Symptoms:

May include nausea, vomiting, low-grade

fever, tachycardia, hypotension, basilarcrackles, abdominal tenderness, rigidity,and diminished bowel sounds.

Acute Pancreatitis: Physical Findings



Acute Pancreatitis: Physical Findings A palpable upper abdominal mass is often present.

Tenderness with guarding and rebound upperabdomen

Cullen’s Sign (blue discoloration about the umbilicus

is a sign of intraperitoneal bleeding) Turner’s Sign (discoloration of the flanks due to

tissue catabolism of hemoglobin) are often present inacute hemorrhagic pancreatitis, a form of pancreatitisthat causes hemorrhage into the pancreatic tissue

Cardiovascular collapse or respiratory distress insevere cases



Acute Pancreatitis: Differential Diagnosis

Cholecystitis

Myocardial

Ischemia Myocardial

Infarction

Pancreatitis Peptic Ulcer

Reflux Esophagitis

Acute Pancreatitis: Clinical Decision Making

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The amylase and lipase are elevated.

In acute pancreatitis, amylase is often elevatedmore than three times normal within a few hours of onset and remains elevated for threedays.

Amylase > 1,000 IU in absence of GIperforation makes diagnosis very likely

After twenty-four hours, serum lipase levels rise

and remain elevated for ten days. Ultrasound often does not visualize the pancreas

because of overlying gas but may detect

gallstones.




cu e c e s: c ec s o g

Assessment of Severity

3 or more of the following abnormalitiesoccurring in the first 48 hours of onset indicatessevere pancreatitis

Calcium <2.0mmol/l

Urea >16mmol/l LDH >600u/l Glucose >10mmol/l PaO2 < 60mmHg WBC >15x109/l

Albumin <32g/l Age >55years

Acute Pancreatitis: Treatment & Management



Hospital Referral

Management may include analgesics and IV fluids, Antibiotics if infection established, NPO.

Surgery indicated for pancreatic abscess orpseudocyst.

Acute Respiratory Distress Syndrome may resultfrom acute pancreatitis or by associated sepsis andhypovolemia.

Pancreatic exudates are thought to destroy thesurfactant.

Hypokalemia and Hyperglycemia are common

complications of pancreatitis.



Pancreatitis Education

Home instructions include a low-fat, no-alcohol, and no-caffeine diet.

Limiting fat intake and avoiding alcoholhelps prevent stimulation of the pancreas.

No caffeine prevents stimulation of gastric

acid that activates the pancreas. 90% of the cases subside after three to

seven days.

Peptic Ulcer Disease: (PUD)



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10% of U.S. population suffers from peptic ulcerdisease. $6 billion in the USA each year in direct

costs of treatment of peptic ulcer disease Peptic ulcers can develop in the lower esophagus,

stomach, pylorus, duodenum or jejunum

80% of peptic ulcers are duodenal ulcers Most common in men between ages 20 to 50.

Gastric Ulcers affect the stomach mucosa are most

common in people ages 55 to 70 (chronic users of NSAIDs or ETOH)

5% to 10% of patients develop complications thatnecessitate surgery.

PUD: Etiology & Pathophysiology



PUD: Etiology & Pathophysiology There are 3 recognized major causes of PUD

Infection with Helicobacter Pylori (gram-negative spiral microaerophilic bacterium)

NSAIDs

Pathologic hypersecretory states such asZollinger-Ellison Syndrome

An imbalance exists between aggressive factors

such as gastric acid and defensive factors thatenhance mucosal integrity such as mucus,prostaglandins, growth factors, blood flow,

bicarbonate, and cell turnover

PUD: Predisposing Factors



PUD: Predisposing Factors

Include blood type:

Gastric Ulcers tend to strike people with type A Blood

Duodenal ulcers tend to afflict people with

type O Blood Exposure to irritants such as alcohol and

tobacco

Physical trauma Emotional stress

Normal aging

PUD: Signs & Symptoms



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Clinical Features vary with the area of the GI tractthat is affected:

GASTRIC ULCERS:

Heartburn, Indigestion

Eating food may relieve pain (food stretches thegastric wall)

Feeling of fullness and distention

Associated Signs & Symptoms:

Weight Loss

Repeated episodes of massive GI Bleeding

Nausea & Vomiting

PUD: Signs & Symptoms



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DUODENAL ULCERS:

Heartburn: Mid-epigastric pain

Usually occurs 2 hours after meals or afterconsumption of orange juice, coffee, aspirin orETOH

Pain is relieved by food, antacids or antisecretory agents

Associated Signs & Symptoms:

Weight gain (patient eats to relieve pain)

Sensation of hot water bubbling in back of throat

Nausea & Vomiting



PUD: Physical Findings

Uncomplicated PUD:

Little more than epigastric tenderness

Complicated PUD:

Rigid Abdomen (perforation)

Hematemesis and melena Patient lies still

Liver dullness may be lost

PUD: Differential Diagnosis



PUD: Differential Diagnosis

Gastroesophageal Reflux Disease (GERD)

Gastric cancer Gastroduodenitis

Cholecystitis

Biliary tract disease Pancreatic cancer

Pancreatitis

Intestinal ischemia Myocardial Ischemia

Non-Nuclear Dyspepsia

PUD: Clinical Decision Making



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Biopsy to rule out H-pylori infection or cancer

Serologic H-pylori or carbon isotope urea breath

tests Serial fecal occult blood tests

Hemoglobin and Hematocrit (values decrease in

GI bleeding) Elevated fasting serum Gastrin and secretin

stimulation test indicates Zollinger-Ellison

Syndrome. Esophagogastroduodenoscopy (EGD) or

Upper gastrointestinal (UGI) series (mucosalabnormalities)

PUD: Treatment & Management



Non-Pharmacological Therapy:

Bed rest, cessation of smoking and ETOH

Discontinuation of NSAID use

Pharmacological Treatment options:

Acid suppression and a combination of antibiotics:(3 drugs twice per day for 7 to 10 days)

Drug combinations include:

Metronidazole, omeprazole, and clarithromycin Lansoprazole, amoxicillin and clarithromycin

Ranitidine, bismuth citrate, amoxicillin and

clarithromycin





A prostaglandin analogue (misoprostol) forpatients taking NSAIDs

A histamine-2 (H2) receptor antagonist(cimetidine or nizatidine) or omeprazole may

reduce acid secretion.

Anti-ulcer drugs: H2-receptor antagonists(ranitidine, nizatidine), antacids (aluminum

hydroxide) or sucralfate for 2 weeks.

Patient responsive: treat for 8 weeks

Non-responsive: diagnostic studies are indicated

PUD: Patient/Family Education/Referral



Advice patient who uses antacids, HX of cardiac

disease or follows a Na restricted diet, to takeantacids that contain low amounts of sodium

Tell patient to avoid hot spicy and high fat foods

Warn patient to avoid steroids, aspirin, NSAIDs,coffee, smoking, ETOH, and stressful situations

Inform patient about potential adverse effects of

antibiotic therapy (superinfection, diarrhea). GI referral for patients with nonresponsive or

recurrent symptoms or for evidence of bleeding

Follow-up patient in 2 weeks for evaluation

Gastroenteritis



Gastroenteritis is an inflammation of the

stomach caused by a virus, bacteria, parasite,or chemical agent.

Signs & Symptoms: N/V/D, abdominal

cramps, hyperactive bowel sounds Associated Signs & Symptoms:

Occasionally fever

Management: symptomatic relief withantiemetics, analgesia, fluid replacement, andtreatment of the underlying cause.

Predisposing Factors Symptoms & Therapy of GI Infections



Pathogen: Predisposing Factors: S/S: DX: TX:

Salmonella Contaminated N/V/D Fecal Ampicillin,

poultry, raw milk, cramps, leukocytes, TMP-SMX,

custards & creams fever, stool chloramphenicol,

foreign travel tenesmus culture ciprofloxacin

Incub:12-36 hrs

Shigella Contaminated food Fever, Fecal TMP-SMX,

foreign travel cramps, leukocytes ciprofloxacin,

tenesmus, tetracycline,

dysentery chloramphenicol,

Incub: norfloxacin

12-24 hrs





Clostridium Antibiotics mild/severe C. difficile Metronidazole,

Difficile antineoplastics diarrhea, toxin & vancomycin,

cramps culture bacitracin, binding

resins

Staph food Contaminated N/V/D Stool Supportive only

poisoning meat, milk, foods onset <4 hr culture

resolves:

24-48 hr

Incub:2-4 hr





Travelers’ Contaminated food N/V/D, Stool TMP-SMX,

Diarrhea vegs, cheese, water cramps, Culture bismuth sub-(E-coli) Incub: salicylate,

16-48 hr doxycycline pro-

phylaxis,

ciprofloxacin,

norfloxacin,

Ofloxacin

E-coli Beef, raw milk, Diarrhea Stool Ciprofloxacin, water H/A, Culture doxycycline,

bloody BM on Mac- TMP-SMX

Incub: Conkey’s

48-96 hrs sorbitol





Viral Community wide N/D, Special Supportive Only

Gastro- outbreaks, cramps viral

Enteritis contaminated food self-limited studies

Campylo- Daycare centers, Diarrhea, Fecal Erythromycin,

bacter contaminated eggs, fever, leukocytes tetracycline,raw milk, foreign malaise Stool ciprofloxacin,

travel Incub: 72 hr Culture chloramphenicol

Cryptos- Immuno- Diarrhea Stool Paromomycin,

Poridosis suppression large fluid Culture, spiramycinDaycare Centers, loss Small

contaminated water Bowel

animal handlers Biopsy

Research & Related Literature

I R h St d i ti t f d th t h



In a Research Study, scientists found that humanintestinal cells with excess iron were more susceptible

to attack by bacteria that cause infection of the smallintestine.

Researchers exposed cells to a common form of iron

that is present in iron supplements. Iron-laden cells were then exposed to Salmonella

enteritidis.

Findings were that cells containing high levels of iron were more easily invaded by the bacteria

Greater numbers of bacteria survived inside cells with

high iron than cells with normal amounts of iron.

Research Study: Iron



y Cells with elevated levels of iron also synthesized

higher amounts of cytokines and chemokines -classes of defense proteins -- in response tobacterial infection.

The secretion of many of these proteins is

associated with the development of inflammation.

The finding suggests that excess iron in theabsorptive cells in the gut may increase both therisk of infection and damage other tissues in theintestine in response to the greater degree of inflammation.

Research Study: Iron

T t i l d th h t



To prevent iron overload, the researchers suggesta revision of the standard policy of iron

fortification of the general population. They recommend periodic evaluation of the iron

status of individuals, particularly women in thereproductive period of their life cycle.

Researchers are planning further experiments toexplain why intestinal cells with high iron levelsare more readily infected.

The study suggests that enriching breakfastcereals and other foods with high doses of iron -a nutritional strategy, could be causing otherhealth problems.

Research: Sulphasalazine & Mesalazine



A Research Study was conducted to determine whether serious adverse effect profiles differ forsulphasalazine and mesalazine.

Sulphasalazine and mesalazine are 5- Aminosalicylates that are extensively prescribed

for the treatment of ulcerative colitis but have a wide range of described adverse effects

Adverse effect profiles were categorized for

interstitial nephritis, pancreatitis, serious skinreactions, hepatitis and hepatic failure, andblood dyscrasias.





Report rates were calculated using prescribing

data from the Department of Health andcompared for mesalazine and sulphasalazine.

Further analysis was undertaken for

sulphasalazine according to disease indication of inflammatory bowel disease or rheumatoidarthritis.

Methods: Analysis of suspected serious adversereactions reported to the Committee on Safety of Medicines of the UK in 1991 – 1998.

Research Results: Sulphasalazine & Mesalazine



A total of 4.7 million prescriptions were dispensedfor sulphasalazine compared with 2.8 million formesalazine.

Interstitial nephritis was only described formesalazine, with 11.1 reports per million

prescriptions.

Pancreatitis was reported 7 times as frequently formesalazine (7.5 per million prescriptions) compared

with sulphasalazine (1.1 per million prescriptions)

There were no reports of serious skin disorders inpatients prescribed sulphasalazine for IBD.




Blood dyscrasias were reported significantly moreoften in patients receiving sulphasalazine for

rheumatoid arthritis than for IBD and there was asimilar trend for hepatic disorders.

Conclusions: Spontaneous reports suggest that

within the five sets of disorders considered, there isno evidence to indicate a safety advantage of mesalazine over sulphasalazine in the treatment of inflammatory bowel disease.

Pancreatitis and interstitial nephritis appearsignificantly more common with mesalazine, andadvice on renal monitoring in patients who receive

mesalazine may need reinforcing.

A Q ti ?



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