HEPATITIS B--HBV
HEPATITIS C--HCV
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APPENDICITIS |
PERITONITIS |
GASTROENTERITIS |
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ETIOLOGY: |
ETIOLOGY: |
ETIOLOGY: |
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SIGNS & SYMPTOMS: |
SIGNS & SYMPTOMS: |
SIGNS & SYMPTOMS: |
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PAIN--EPIGASTRIC, PERIUMBILICAL; LATER: RLQ(MCBURNEY'S POINT); N & V FOLLOW |
PAIN IS DIFFUSE AND SEVERE; LEGS ARE DRAWN UP; N & V |
PAIN: N & V OCCUR FIRST, THEN PAIN IS GENERALIZED |
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GUARDING, REBOUND TENDERNESS |
RIGIDITY, DISTENTION, HYPOACTIVE B. S., HICCUPS |
HYPERACTIVE B. S., DIARRHEA |
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TEMP--WNL OR SLIGHTLY ELEVATED |
FEVER, CHILLS, DEHYDRATION, THIRD SPACING |
FEVER |
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LEUKOCYTOSIS<20K--"SHIFT TO THE LEFT" |
LEUKOCYTOSIS>20K--"SHIFT TO THE LEFT"; CHEM 7, H&H, ABGS, BLOOD CULTURES |
STOOL FOR GRAM STAIN OR CULTURE |
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XRAY: FREE AIR IN PERITONEAL CAVITY |
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COMPLICATIONS |
COMPLICATIONS |
COMPLICATIONS |
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PERITONITIS |
SEPTICEMIA; RESPIRATORY FAILURE; RENAL FAILURE |
HYPOVOLEMIC SHOCK |
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TREATMENT |
TREATMENT |
TREATMENT |
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SURGICAL: MAY BE DONE WITH LAPAROSCOPY OR OPEN ABDOMINAL INCISION |
SURGICAL: EXPLORATORY "LAP" & TREAT UNDERLYING CAUSE: MAY INCLUDE SHOCK MANAGEMENT WITH FLUID RESUSCITATION, ANTIBIOTICS, N/G TUBE, O2 THERAPY, ICU |
SUPPORTIVE & ANTI-INFECTIVES FOR CAUSATIVE ORGANISM |
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NURSING CARE: GENERALLY, POST-OP CARE OF A PATIENT FOLLOWING ABDOMINAL SURGERY |
CRITICAL CARE WITH HEMODYNAMIC MONITORING AND, POSSIBLY, MECHANICAL VENTILATION |
MEDICAL CARE OF PT. WITH FLUID AND ELECTROLYTE DEFICITS; ISOLATION PRECAUTIONS |
1. INCIDENCE: 600,000 CASES IN U.S.(FOR BOTH)
2. CLASSIFICATIONS:
A. MILD DISEASE--REQUIRES SYMPTOMATIC RELIEF AND DIETARY MANIPULATION
C. SEVERE DISEASE--STEROIDS, IMMUNOSUPPRESSANTS, SURGERY
3. ETIOLOGY: GENETIC VS ENVIRONMENT
4. PATHOPHYSIOLOGY:
CROHN'S DISEASE INVOLVES THE ENTIRE G.I. TRACT, WITH DISCONTIUNOUS FOCAL ULCERATION, FISTULA FORMATION AND PERIANAL INVOLVEMENT; THE TERMINAL ILEUM IS MOST COMMONLY AFFECTED WITH VARIABLE DEGREES OF COLONIC INVOLVEMENT.
ULCERATIVE COLITIS IS CHARACTERIZED BY SHALLOW, CONTINUOUS INFLAMMATION EXTENDING FROM THE RECTUM PROXIMALLY TO INCLUDE THE ENTIRE COLON. THERE IS AN INCREASED RISK FOR COLON CANCER. SMALL BOWEL INVOLVEMENT IS ABSENT.
5. SIGNS & SYMPTOMS
6. DIAGNOSED BY COLONOSCOPY, FLEXIBLE SIGMOIDOSCOPY, BARIUM ENEMA, STOOL STUDIES, LAB STUDIES SUCH AS CBC, ESR, ELECTROLYTES
(1) 5-AMINOSALICYLIC ACID COMPOUNDS( DIPENTUM, ASACOL, PENTASA, ROWASA) ARE TOPICALLY EFFECTIVE ANTI-INFLAMMATORYAGENTS. SIDE EFFECTS ARE RARE. DRUGS IN THIS CATEGORY COME IN ORAL FORMS, ENEMAS AND SUPPOSITORIES.
(2) ANTIBIOTICS: MOST STUDIED IN CROHN'S DISEASE; METRONIDAZOLE (FLAGYL) AND CIPROFLOXACIN (CIPRO) HAVE BEEN USED WITH GOOD THERAPEUTIC EFFECT.
(3) CORTICOSTEROIDS:
(a) SYSTEMIC--PREDNISONE 40-60MG DAILY OR HYDROCORTISONE 100 MG EVERY 8 HRS. IMPROVEMENT OVER 6 TO 8 DAYS. THEN, TAPER DRUGS.
(b) TOPICAL--CORTICOSTEROID ENEMAS BENEFIT PATIENTS WITH ULCERATIVE PROCTOSIGMOIDITIS. COME I N FOAM AND LIQUID.
NOT AS EFFECTIVE AS 5-ASA ENEMAS.
(4) IMMUNOSUPPRESSANT DRUGS:
ASATHIOPRINE (IMURAN) OR MERCAPTOPURINE (PURIENTHOL) ARE USED--TAKE UP TO 3 MONTHS FOR BEST BENEFIT; HAVE BEEN MORE STUDIED IN CROHN'S DISEASE. INITIAL DOSAGE IS 50 MG DAILY. BLOOD COUNT IS NECESSARY EVERY TWO WEEKS AT FIRST AND THEN EVERY THREE MONTHS FOR MAINTENANCE.
METHOTREXATE (RHEUMATREX) ALSO USED. GIVEN AS I.M. INJECTION WEEKLY IN DOSE OF 15 TO 25 MG. CBC, CHEST XRAY,LIVER FUNCTION AND RENAL FUNCTION SHOULD BE DONE AND MONITORED CLOSELY; LIVER BIOPSY IS INDICATED IN PATIENTS WITH ABNORMAL LIVER FUNCTION TESTS.
CYCLOSPORINE(SANDIMMUNE) IS USED IN SEVERELY ILL PTS. WITH ULCERATIVE COLITIS WHO HAVE NOT RESPONDED TO STEROIDS. SIDE EFFECTS ARE NEPHROTOXICITY AND HYPERTENSION.
INTERLEUKIN 10 AND INTERLEUKIN 11 HAVE BEEN FOUND TO BE OF BENEFIT IN CROHN'S DISEASE.
(5) LOPERAMIDE(IMODIUM) OR CHOLESTYRAMINE(QUESTRAN) TO HELP WITH DIARRHEA
(1) LACTOSE-FREE
(2) LOW FIBER
(3) VITAMIN SUPPLEMENTATION--MAY NEED VITAMIN B12, FOLATE OR IRON; IF ANEMIA DOES NOT RESPOND TO IRON REPLACEMENT, THEN EPOGEN (SYNTHETIC ERYTHROPOIETIN) IS USED TO STIMULATE RBC PRODUCTION
(4) WITH ACTIVE DISEASE OR "SHORT BOWEL SYNDROME", TPN IS NECESSARY EITHER IN THE HOSPITAL OR AT HOME. PT. IS NPO TO ALLOW THE BOWEL TO REST.
(1) TOTAL PROCTOCOLECTOMY WITH PERMANENT ILEOSTOMY
(2) KOCK'S ILEOSTOMY
(3) ILEOANAL ANASTAMOSIS
(1) OSTOMY & SKIN CARE
(2) DIET MODIFICATIONS
(3) MEDICATIONS
(4) SIGNS & SYMPTOMS TO REPORT TO THE DOCTOR
(5) STRESS MANAGEMENT
D. REFERRAL TO RESOURCES
1. DEFINITION AND LOCATION:
ABNORMAL OUTPOUCHINGS IN THE WALL OF THE INTESTINES--MORE COMMONLY LOCATED IN THE LLQ(SIGMOID).
2. PATHOPHYSIOLOGY:
OBSTRUCTION CAUSES INFLAMMATION, RUPTURE, ABSCESS FORMATION, HEMORRHAGE, FISTULAS
3. RISK FACTORS:
INCREASING AGE AND LOW FIBER DIET
4. SIGNS & SYMPTOMS:
5. LABS:
USUALLY DISCOVERED INCIDENTALLY WITH G.I. XRAYS; WBCS ARE ELEVATED, STOOL MAY BE GUAIAC POSITIVE. NO BARIUM STUDIES OR SIGMOIDOSCOPY SHOULD BE DONE WITH ACUTE DISEASE, AS THIS MAY CAUSE PERFORATION. FLAT PLATE OF ABDOMEN MAY SHOW FREE AIR UNDER DIAPHRAGM INDICATING PERFORATION OR CT SCAN WILL SHOW ABSCESS. ULTRASOUND WILL ALSO SHOW THIS.
6. TREATMENT:
GOAL: INCREASED TISSUE PERFUSION TO BOWEL
A. NONSURGICAL INTERVENTIONS MAY INCLUDE NPO STATUS, I.V.S, ANTIBIOTICS, N/G TUBE, ANALGESIA, ANTICHOLINERGICS TO REDUCE INTESTINAL HYPERMOTILITY. WHEN PT. CAN RESUME EATING, A LOW RESIDUE DIET IS ORDERED WITH TEACHING ABOUT RESUMING A HIGH FIBER DIET WHEN DISCHARGED FOR PREVENTION OF FURTHER EPISODES.
B. SURGICAL TREATMENT IF COMPLICATIONS OCCUR; CARE IS SAME AS FOR BOWEL RESECTION AND COLOSTOMY
C. TEACHING: DIET MODIFICATIONS, COLOSTOMY AND SKIN CARE, AVOIDANCE OF LAXATIVES OTHER THAN BULK FORMING TYPES AND AVOIDANCE OF ACTIVITIES THAT CAUSE INCREASED ABDOMINAL PRESSURE SUCH AS STRAINING, BENDING OR LIFTING HEAVY OBJECTS; TEACH SIGNS AND SYMPTOMS TO REPORT TO M.D.
D. REFERRAL TO SUPPORT GROUPS
1. INCIDENCE:
MOSTLY WOMEN, BETWEEN 20-50 YRS. OF AGE. MEN AFTER 50. DIABETES, BCP, PREGNANCY, SEDENTARY LIFE STYLE, OBESITY, AND HI FAT OR STARVATION DIETS MAY BE PRECIPITATING FACTORS. THERE IS A FAMILIAL TENDENCY.
2. PATHOPHYSIOLOGY:
ACUTE CHOLECYSTITIS: STONES FORM, CAUSING BLOCKAGE OF BILE DRAINAGE FROM GALLBLADDER; INFLAMMATION OCCURS, BUT OBSTRUCTION IS NOT USUALLY ENOUGH TO CAUSE JAUNDICE
CHRONIC CHOLECYSTITIS : INEFFICIENT EMPTYING; MAY COME BEFORE OR AFTER STONE FORMATION AND PERSIST.
INFLAMMATION IS FOLLOWED BY FIBROSIS
OBSTRUCTIVE JAUNDICE COMMON; CHOLANGITIS AND PANCREATITIS OFTEN RESULTS.
3. SIGNS & SYMPTOMS:
4. LABS & STUDIES:
WBCS ELEVATED, SED RATE ELEVATED, IF BILE OBSTRUCTION AND JAUNDICE, THEN BILIRUBIN ELEVATED(DIRECT MORE THAN INDIRECT), ALKALINE PHOSPHATASE(ALP) ELEVATED; POSITIVE ULTRASOUND OR POSSIBLY HIDA SCAN IS DONE; CHOLANGIOGRAM MAY BE DONE
5. COMPLICATIONS:
ABSCESS, PERITONITIS
6.TREATMENT:
DRUGS TO "DISSOLVE" STONES TAKE YEARS OR LITHOTRIPSY TO BREAK UP STONES HAS FALLEN OUT OF FAVOR, SO SURGERY IS PREFERRED APPROACH
A. CHOLECYSTECTOMY--"LAP CHOLE" PREFERRED AS FIRST CHOICE, WITH TRADITIONAL OPEN METHOD AS BACKUP; LAP CHOLE NOT USED FOR PTS. WHO HAVE HAD EXTENSIVE ABD SURGERY, SEVERE SYMPTOMS OR PALPABLE GALL BLADDER
NURSING CARE WITH LAP CHOLE:
MODIFICATIONS WITH TRADITIONAL OPEN APPROACH:
B. CHOLEDOCHOLITHOTOMY:
CBD (COMMON BILE DUCT EXPLORATION) TO REMOVE STONES--T TUBE LEFT IN CBD AS SPLINT AND AS A MEASURE TO DRAIN BILE FROM THE AREA UNTIL SWELLING OF CBD DECREASES AND LUMEN IS OPEN ENOUGH TO ADEQUATELY DRAIN BILE INTO THE SMALL INTESTINE
CARE OF PT. WITH T TUBE:
C. DIET THERAPY:
INSTRUCT PT. ON LOW FAT DIET, BUT PT. WILL INCLUDE OR EXCLUDE FOODS ACCORDING TO HIS/HER TOLERANCE; SOME PTS. MAY BENEFIT FROM EATING SEVERAL SMALLER MEALS THROUGHOUT THE DAY RATHER THAN THREE LARGE MEALS
D. OTHER DISCHARGE INSTRUCTIONS CENTER AROUND ACTIVITY RESTRICTIONS, MEDICATION INSTRUCTION, WOUND INSPECTION FOR INFECTION, SIGNS AND SYMPTOMS TO REPORT TO M.D. AND WHEN TO RETURN TO WORK AND FOR FOLLOW UP
1. TWO FUNCTIONS OF THE PANCREAS:
A. EXOCRINE--RELEASE OF ENZYMES SUCH AS PROTEASE, LIPASE AND AMYLASE FOR DIGESTIONS OF PROTEIN, FAT, AND CHO
B. ENDOCRINE--INSULIN SECRETION FROM BETA CELLS AND GLUCAGON FROM ALPHA CELLS
2. ACUTE PANCREATITIS IS A DISORDER OF THE EXOCRINE FUNCTION AND ENZYMES START TO AUTODIGEST THE ORGAN AND EVENTUALLY SURROUNDING TISSUES; ETIOLOGY IS MOST OFTEN BILIARY DISEASE OR ALCOHOLISM. HYPERCALCEMIA ALSO CAN CAUSE CALCIUM STONE FORMATION IN THE PANCREATIC DUCT OBSTRUCTING IT. ONSET OF THIS DISORDER IS SUDDEN AND SEVERE, AND MAY BE LIFE- THREATENING.
3. CHRONIC PANCREATITIS-- RECURRENT FLARE UPS OF INFLAMMATION WITH PROGRESSIVE DESTRUCTION OF PANCREATIC TISSUE AND FUNCTION.
USUALLY CAUSED BY CHRONIC ALCOHOLISM. FIBROSIS AND CALCIFICATION OF PANCREATIC TISSUE RESULTS.
4. MAIN S&S:
HALLMARK IS EXCRUCIATING PAIN IN EPIGASTRIC OR LUQ WITH RADIATION TO BACK OR FLANKS, NAUSEA, VOMITING, JAUNDICE, FLANK DISCOLORATION(GREY TURNER'S SIGN), UMBILICAL DISCOLORATION (CULLEN'S SIGN), ABDOMINAL DISTENTION, PARALYTIC ILEUS, FEVER, HYPOCALCEMIA, HYPOKALEMIA, HYPOMAGNESEMIA, HYPOALBUMINURIA CAUSING THIRD SPACING OF FLUID, LOWERED RESISTANCE TO . INFECTION AND IMPAIRED GLUCOSE TOLERANCE
5. LABS: INCREASED AMYLASE AND LIPASE, ELEVATED URINE AMYLASE, HYPERGLYCEMIA, HYPOCALCEMIA, HYPOKALEMIA, HYPOMAGNESEMIA, INCREASED WBCS, ELEVATED ALP AND BILIRUBIN, STEATORRHEA
6. OTHER STUDIES: ERCP (ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY) SHOWS DUCTAL DEFORMITY OR RETAINED COMMON BILE DUCT STONES
7. COMPLICATIONS: RESPIRATORY FAILURE, LEFT PLEURAL EFFUSION, ABSCESSES, FISTULAS, PERITONITIS, HEMORRHAGE, SHOCK, PSEUDOCYSTS--ENCAPSULATED, SAC-LIKE STRUCTURES THAT FORM ON OR SURROUND THE PANCREAS; THEY USUALLY REQUIRE SURGICAL DRAINAGE.
8. MEDICAL TREATMENT AND NURSING MANAGEMENT:
(A TEAM OF PRIMARY PHYSICIAN, GASTROENTEROLOGIST, PAIN MANAGEMENT PERSONNEL, METABOLIC SUPPORT PERSONNEL, CHEMICAL DEPENDENCY COUNSELORS, NURSING, RESPIRATORY THERAPY AND DIETARY PERSONNEL)
A. NPO WITH N/G SUCTION, I.V. FLUIDS AND ELECTROLYTE REPLACEMENT(E.G., K PROTOCOL); TPN FOR ADEQUATE NUTRITION WITH DAILY WEIGHTS; MONITOR FOR SHOCK; MONITOR FOR D.T.S
B. PAIN MANAGEMENT--NARCOTICS(NO MORPHINE) FOR ACUTE, NON- NARCOTICS FOR CHRONIC
C. DRUG THERAPY TO INCLUDE ANTIPYRETICS, ANTIBIOTICS, H2 BLOCKERS, ANTACIDS
D. BLOOD SUGAR MONITORING AND SLIDING SCALE INSULIN
E. O2 THERAPY WITH ACUTE; MONITOR FOR RESPIRATORY FAILURE
F. GIVE BLOOD PRODUCTS AS NECESSARY(PACKED RBCS OR ALBUMIN)
G. EMOTIONAL SUPPORT
H. DIETARY THERAPY: NO ALCOHOL OR CAFFEINE; BLAND, HIGH PROTEIN, LOW FAT--GIVE REPLACEMENT ORAL PANCREATIC ENZYMES (VIOKASE, ILOZYME) WITH SIX SMALL MEALS A DAY TO STOP STEATORRHEA
I. MONTHLY FOLLOW UP: REFERRAL TO AA IF INDICATED
J. SURGERY FOR COMPLICATIONS
1. HIGHLY MALIGNANT AND WHEN DISCOVERED, THIS CANCER IS IN A LATE STAGE. 5TH LEADING CAUSE OF CANCER-RELATED DEATHS IN U.S. ONLY ABOUT 3% ARE ALIVE 5 YESRS AFTER DIAGNOSIS. HIGH RATES IN AFRICAN AMERICANS AND SMOKERS.
2. HEAD OF PANCREAS IS THE MOST COMMON SITE; JAUNDICE IS A PROMINENT SYMPTOM DUE TO COMPRESSION OF BILIARY TREE. THROMBOPHLEBITIS IS COMMON DUE TO INCREASED THROMBOPLASTIC FACTORS IN THE BLOOD.
3. CEA (CARCINOEMBRYONIC ANTIGEN) IS ELEVATED IN 80 TO 90% OF PTS.
4. TREATMENT: PALLIATIVE WITH RADIATION AND CHEMO; PAIN CONTROL WITH DILAUDID
SURGERY: CAN BE DONE WITH HOPE OF A CURATIVE RESECTION; A TOTAL PANCREATECTOMY OR WHIPPLE PROCEDURE IS TRIED, BUT PT IS VERY ILL THEREAFTER WITH MANY PROBLEMS SUCH AS POTENTIAL FOR FISTULA FORMATION, SHOCK, HYPERGLYCEMIA, AND NEGATIVE NITROGEN BALANCE. THIS IS A VERY RADICAL SURGERY.
2. PATHO: DIRECT TOXIC EFFECT-->INFLAMMATION-->FATTY INFILTRATION AND SCARRING-->HEPATOMEGALY-->PROGRESSIVE DAMAGE TO HEPATIC PARENCHYMA AS RESULT OF MALNUTRITION AND REPEATED EXPOSURE TO ALCOHOL-->FIBROSIS-->LIVER SHRINKS AND BECOMES "HOBNAIL"
3. LABS: LFTS: AST, ALT, LDH, ALP ELEVATED; BILIRUBIN ELEVATED; PROLONGED PROTHROMBIN TIME OR INR; ELEVATED BLD. AMMONIA(HEPATIC COMA)
4. METABOLIC ABNORMALITIES RESULT:
PERSISTENT INCREASE IN PRESSURE WITHIN THE PORTAL VENOUS SYSTEM AS BLOOD MEETS RESISTANCE TO FLOW AND SEEKS COLLATERAL VENOUS CHANNELS AROUND THE HIGH- PRESSURE AREA. BACK UP INTO THE SPLEEN (SPLENOMEGALY), ESOPHAGUS (ESOPHAGEAL VARICES), AND ABDOMEN(ASCITES).
MANIFESTATIONS OF ASCITES:
INCREASING ABDOMINAL GIRTH, PROTRUDING UMBILICUS, HERNIAS, ORTHOPNEA, DYSPNEA; AGGRAVATED BY INABILITY OF LIVER TO PRODUCE SUFFICIENT ALBUMIN
TREATMENTS AND NURSING CARE:
(1)PARACENTESIS--WATCH FOR SHOCK
(2) DIET THERAPY--LOW NA, FLUID RESTRICTION, VITAMIN SUPPLEMENTS SUCH AS FOLATE, THIAMINE AND MULTIVITAMINS
(3) DRUG THERAPY--DIURETICS SUCH AS SPIRONOLACTONE (ALDACTONE) AND LOOP DIURETICS WITH POTASSIUM SUPPLEMENTS;SALT POOR ALBUMIN; SALT FREE ANTACIDS (RIOPAN)
(4) SHUNTS(LEVEEN OR DENVER )--BYPASS THE PORTAL SYSTEM AND DIVERT FLUID TO VENA CAVA; LAST DITCH MEASURE AS THESE PTS. ARE HIGH RISK; T. I. P. S.(TRANSJUGULAR INTRAHEPATIC PORTAL-SYSTEMIC SHUNT) LESS INVASIVE AND FAR SAFER THAN SURGERY AND GENERAL ANESTHESIA; AFTER SHUNTING, MONITOR WEIGHT, ABDOMINAL GIRTH AND URINARY OUTPUT TO CHECK EFFECTIVENESS
FAT SOLUBLE VITAMINS LIKE VITAMIN K ARE NOT ABSORBED, SO CLOTTING FACTORS ARE INSUFFICIENT.
MANIFESTATIONS: EASY BRUISING, G.I. BLEEDING
TREATMENTS AND NURSING CARE:
(1) GIVE VITAMIN K AS ORDERED
(2) MONITOR CLOTTING TIMES
(3) GUAIAC STOOLS
(4) GIVE H2 BLOCKERS & ANTACIDS
(5) TREAT ACTIVE ESOPHAGEAL VARICES:
INTERVENTIONS:
a. INSERTION OF SENGSTAKEN-BLAKEMORE TUBE OR MINNESOTA TUBE (ESOPHAGOGASTRIC BALLOON TAMPONADE):
MONITOR PRESSURE OF ESOPHAGEAL BALLOON
PT. CAN'T SWALLOW--SUCTION SECRETIONS AS NECESSARY
ICE WATER LAVAGE TO CONTROL BLEEDING
SEDATION & TRACTION ON THE TUBE
ATTACH TO LOW INTERMITTENT GASTRIC SUCTION
MONITOR PATIENT FOR RESPIRATORY DISTRESS IF THE ESOPHAGEAL BALLOON BECOMES DISPLACED UPWARD COMPRESSING THE AIRWAY
b. SCLEROTHERAPY OR LIGATION--DONE THROUGH ENDOSCOPY
INJECTION--USE OF A SCLEROSING AGENT TO STOP BLEEDING
LIGATION--USE OF BANDS TO LIGATE THE BLEEDING VARICES
c. PITRESSIN DRIP (VASOPRESSIN)
DRUG CAUSES VASOCONSTRICTION OF BLEEDING VESSELS AND DECREASES BLOOD FLOW TO ABDOMINAL ORGANS, REDUCING PORTAL PRESSURE AND PORTAL BLOOD FLOW
MONITOR B/P, PULSE, INTAKE AND OUTPUT; ASSESS FOR DEVELOPMENT OF CHEST PAIN, CARDIAC DYSRHYTHMIAS AND ABDOMINAL CRAMPING
MAY CAUSE ANGINA OR M.I. IN PATIENT WITH CORONARY ARTERY DISEASE; NITROGLYCERIN DRIP MAY PREVENT THIS
d. GIVE BLOOD PRODUCTS AS NECESSARY
e. T.I.P.S.--SHUNT PLACED BETWEEN PORTAL AND HEPATIC VEIN TO REDUCE PORTAL VENOUS PRESSURE AND THUS CONTROL BLEEDING
PORTACAVAL SHUNT OR SPLENORENAL SHUNT -->HI MORTALITY
LIVER CANNOT METABOLIZE BILIRUBIN AND OBSTRUCTION WITHIN THE LIVER CAUSES BILIRUBIN TO ACCUMULATE IN THE BLOOD.
INTERVENTIONS:
(1) MEDS TO CONTROL ITCHING(TEMERIL)
(2) KEEP PT'S FINGERNAILS SHORT
(3) SOOTHING LOTIONS
LIVER CANNOT CONVERT AMMONIA FROM PROTEIN METABOLISM AND BACTERIAL ACTION IN THE G.I. TRACT INTO UREA FOR EXCRETION BY THE KIDNEYS; THEREFORE, AMMONIA BUILDS UP IN THE BLOOD AND AFFECTS THE C.N.S. SOME FACTORS THAT CAN PRECIPITATE PSE INCLUDE HI PROTEIN DIET, INFECTIONS, HYPOKALEMIA AND G.I. BLEEDING.
INTERVENTIONS:
(1) ASSESS FOR ALTERED MENTAL STATUS, ASTERIXIS(LIVER FLAP OR FLAPPING TREMOR) AND FETOR HEPATICUS SIGNALING HEPATIC ENCEPHALOPATHY
(2) LOW PROTEIN DIET
(3) CONTROL G.I. BLEEDING--NPO WITH TPN
(4) PREVENT HYPOKALEMIA
(5) DRUG THERAPY:
a. LACTULOSE(CEPHULAC) --VIA ORAL ROUTE, N/G TUBE OR ENEMAS--LAXATIVE EFFECT TO RID BODY OF AMMONIA THROUGH TWO TO THREE SOFT STOOLS PER DAY; MONITOR FOR EXCESSIVE DIARRHEA, DECREASING AMMONIA LEVELS AND FOR FLUID AND ELECTROLYTE IMBALANCES
b. NEOMYCIN--DESTROYS NORMAL FLORA IN THE BOWEL, DIMINISHING PROTEIN BREAKDOWN AND DECREASING AMMONIA PRODUCTION
(1) SPREAD BY ORAL-FECAL ROUTE BY ORAL INGESTIONS OF FECAL CONTAMINANTS LIKE CONTAMINATED WATER, SHELLFISH OR BY FOOD HANDLERS INFECTED WITH THE VIRUS. CHILDREN ARE A "SILENT SOURCE OF INFECTION". HEPATITIS E IS SPREAD BY SAME METHODS.
(2) INCUBATION PERIOD--AVERAGE OF 4 WKS.
(3) 65% OF ALL HEPATITIS REPORTED IN U.S.
(4) MANIFESTED BY: JAUNDICE, ABDOMINAL PAIN, NAUSEA & VOMITING,
FEVER, CHILLS AND FATIGUE
(5) IDENTIFIED BY: PRESENCE OF ANTIBODIES IN THE BLOOD(ANTI-HAV)
ALT AND AST LEVELS ARE GREATLY ELEVATED
(5) MOST RECOVER IN 3 WEEKS
(6) PREVENTATIVE AFTER EXPOSURE IS IMMUNE GLOBULIN; NOW THERE ARE ALSO VACCINES GIVEN IN TWO DOSES ABOUT SIX TO EIGHTEEN MONTHS APART
(1) SPREAD THROUGH HIGH RISK BEHAVIORS, BLOOD TRANSFUSIONS, DIALYSIS, TATTOOING, BODY PIERCING AND PERINATALLY
(2) INCUBATION PERIOD IS ABOUT 2 TO 6 MONTHS, BUT COMMONLY APPEARS 2 TO 3 MONTHS AFTER EXPOSURE
(3) VERY SMALL PERCENTAGE DEVELOP CHRONIC HEPATITIS B
(4) TENDS TO HAVE MORE SEVERE ACUTE SYMPTOMS THAN HAV
(5) LAB: HBsAG ARE SEROLOGIC MARKERS IN THE BLOOD; CARRIERS ARE POSITIVE FOR THESE MARKERS ALSO
(6) VACCINES ARE AVAILABLE
(1) CHRONIC HCV IS MAJOR REASON FOR LIVER TRANSPLANT IN U. S.
(2) SPREAD BY SAME SOURCES AS HBV
(3) INCUBATION PERIOD ON THE AVERAGE IS SEVEN WKS.
(4) ONLY ONE THIRD OF PATIENTS DEVELOP JAUNDICE OR SYMPTOMS; IF CLINICALLY APPARENT, COURSE OF DISEASE IS 2-12 WEEKS
(5) LABS: ANTI-HCV ANTIBODIES DETECTED IN BLOOD SINCE 1989
(6) MOST OF PTS. DEVELOP CHRONIC HEPATITIS LEADING TO DEVELOPMENT OF CIRRHOSIS AND HIGH RISK FOR LIVER CANCER
(7) TREATMENT: ALPHA INTERFERON--A PROTEIN NATURALLY PRODUCED IN OUR BODIES TO FIGHT VIRUSES BY BOOSTING THE IMMUNE SYSTEM; THE SYNTHETIC MEDICATION GIVEN IS ALSO CALLED "ALPHA INTERFERON".
IN SOME PATIENTS, THIS MED STOPS THE LIVER INFLAMMATION SHOWN BY DECREASE IN LIVER ENZYMES AND MAY RID THE PATIENT OF THE HEPATITIS C VIRUS ALTOGETHER.
GIVEN AS SUBQ INJECTIONS, SELF ADMINISTERED OVER A PERIOD OF WEEKS DEPENDING ON WHETHER ACUTE OR CHRONIC IS BEING TREATED; IT IS CONSIDERED EFFECTIVE IN CHRONIC HVC IF LIVER ENZYMES ARE WNL AFTER EIGHT WEEKS OF TREATMENT. TREATMENT IS THEN CONTINUED FOR ONE YEAR.
RIBAVIRIN--NEW DRUG JUST APPROVED BY FDA
(1) NO ALCOHOL
(2) AVOID ALL MEDICATIONS AND OTC MEDICATIONS ESPECIALLY TYLENOL
(3) GET ADEQUATE REST
(4) NUTRITIOUS DIET OF HIGH CHO, LOW FAT FOODS
(5) AVOID SEX UNTIL ANTIBODY TESTING RESULTS ARE NEGATIVE