What anatomy is on the mind line of the GI system?
Urinary bladder and urethra
Right upper quadrant
Pylorus, duodenum, liver, right kidney and adrenal gland, hepatic flexor of the colon and head of pancreas
Left upper quadrant
Stomach, spleen, left kidney and adrenal gland, splenic flexure of the colon, body of the pancreas
Right lower quadrant
Cecum, appendix, right ovary and fallopian tube, right utter ad lower kidney pole, right spermatic cord
Left lower quadrant
Signmoid colon, left ovary and fallopian tube, left utter and lower kidney pole,, left spermatic cord
Acute GI hemorrhage: upper vs Lower
Upper GI bleed (80%) of acute GI bleed: peptic ulcer disease (gastric, duodenal) 50%, esophageal 10-20%, stress ulcer, malllory-Weiss tear, cancer
Lower GI bleeding 20%-diverticulosis, Angiodysplasia, tumor, radiation, colitis, Crohn’s disease, infectious: c, diff, and E. coli
Which has higher mortality? Upper or lower
Upper
General management of upper GI bleed
Address the cause, isotonic fluid resuscitation as for hypovelmic shock, PRBC, replace clotting factors, (ffp and platelets), medications - vasopressin constricts the splanchnic arteriolar bed, decrease portal venous pressure, watch for Chest pain and st elevation
OctreotideL reduces splanchnic blood flow, gastric acid secretion, and GI motility
Osmotic laxatives:lactulose, remove nitrogenous materials (blood) out of gut to prevent ammonia conversion, important to administer in presence of liver disease
Beta blocker contradict mesenteric arterioles, reducing portal venous flow
Esophageal varies, what is it and its treatment?
Common cause is portal hypertension secondary to liver disease, venous darainge of the GI tract
Liver cirrhosis prevent normal drainage through the liver. Pressure backs p into esopgehal veins-hemorrhoids of the esophagus
Treatment: endoscopy with banding, blakemore tube-gastric balloon attach to suction, empties stomach, 200-500ml
Esophageal balloon 20-40mmhg, used to control bleeding
If displaced up, can occluded the airway
Cut the esophageal balloon if there is respiratory distress
Pancreas exocrine and endocrine functions
Exocrine functions: secretion of bicarbonate to neutralize stomach acid
Digestive enzymes: amylase, lipase, trypsin
Secretions increased by parasympathetic stimulation, ingestion of food (secretin and choleycystokinin)
Endocrine functions: alpha cells- secrete glucagon -hormone to raise blood sugar by telling the liver to release glucose
Beta cells-serete insulin
Delta cells inhibit the secretion of glucagon and insulin
Etiology of acute pancreatitis
Acute pancreatitis is the diffuse inflammation, destruction, and auto digestion of the pancreas from premature activation of exocrine enzymes. It is usually not caused by an infection. Up to 6 L of fluid may be secreted into the intersectional space. Activation of inflammatory mediators, such as kinins, cytokines histamine clotting factors. Results in systemic inflammatory response syndrome, which increases vasodilation, vascular permeability, vascular stasis, and micro thrombosis
Etiology includes alcoholism, obstruction, such as gallstones, abdominal surgery, drugs, hyperlipidemia, trauma, infection
Pulmonary complications of acute pancreatitis
Left lower lobe Atelectasis, left-sided pleasurable effusion, bilateral crackles, ARDS
S/S of acute pancreatitis
Abdominal pain, pain radiating to all quadrants and the lumbar area, nausea, vomiting, rigid abdomen, no rebound tenderness, decreased or absent bowel sounds, low-grade fever, increased white blood cell, increased amylase, lipase increased, decreased calcium, increased blood sugar
Calcium is used up during auto digestion, which cause low calcium, which leads to trousseau’s sign, prolonged qt, and seizures
This sign is when the cuff is inflated, the brachial artery is occluded, the ABSCENCE of bloood flow will cause the muscle of the hand and forearm to have muscle spasm
Beta cell incjury will cause hypeglycemia, can lead to HHS
Phospholipase A is released-this “kills” type 2 alveolar cells, which decreases surfactant, and leads to ARDS
Pancreatic inflammation and capillary leak may block the pancreatic duct and cause left diapgramatic lifting, left Atelectasis, and left pleural effusion
S/s of hemorrhagic pancreatitis
Cullen’s sign-bluish discoloration and ecchymosis or the periumbilical area (cullen’s umbilucus )
In acute pancreatitis, methemalbumin forms from digested blood and tracks around he abdomen from the inflamed pacnreas: this is sign of intra-abdominal bleeding
Grey turner’s sign-bluish discoloration of the flanks (turn the pt o see the flank)-sign of RETROPERITONEAL bleeding
Ranson’s criteria for the severity of acute pancreatitis at admission vs during the next 48 hrs
At admission: age over 55, wbc over 16k, glucose over 200, LDH under 350, ast under 250
Next 48 hrs: hot decreased of 10%, bun increase over 5, fluid sequestration over 6L, calcium under 8, PAO2 under 60, base deficit over 4
Treatment for acute pancreatitis
Fluid replacement
Calcium, k, and mag replacement
H2 blockers or proton pump inhibitor to decrease gastric ph
No suction to decrease gastric secretions
Pain management, morphine
Glucose control
Enteral feeding below the duodenum
Monitor for pulmonary complications
Hepatic failure s/s and labs
Acute hepatic failure- Tylenol od, chronic-alcohol abuse
Labs
Decreased: serum protein, albumin,wbc,rbc,platelets,blood sugar
Increased:nh3, coagulopathies, ast, alt, GTT, serum bilirubin, hyperventilation, resp alkalosis, and met acidosis due to lactate increase, creatinine, bun
S/s
Menta status change
Asterixis (hand tremor) d/t elevated ammonia
As cites did/t low albumin
Jaundice
Renal failure- hepatorenal syndrome
Sepsis d/t decreased immune function
Liver become enlarged and tender
Stages of hepatic encephalopathy
Stage 1-mild confusion,forgetfulness, irritability, changes in sleep patterns, eeg is normal
Stage 2-lethargy, confusion, apathy, aberrant behavior, asterixis, eeg is normal
Stage 3-severe, semi-stupor to stupor, hyperactive deeep tendon reflex, hyperventilation,eeg is abnormal
Stage 4-no response to stimuli, posturing, positive babinski, a reflex is except for pathological reflexes, eeg is abnormal
Factors that increase serum nh3
Hypokalemia: triggers the kidneys
Increased bun: breakdown of nitrogen
Increased protein: breakdown of nitrogen
Increased lactic acidosis : maybe precipitated by the administration of lactate ringers normally converted into bicarb with a healthy liver
Management of hepatic failure
Prevent anything that will increase ammonia and attempt to decrease ammonia
Prevents low potassium. prevent increase BUN. prevent G.I. bleeding because of the breakdown of protein in the gut will increase ammonia, prevent acid buildup do not give administration of lactate ringers
Restrict protein, only if hepatic encephalopathy is present
Administer clotting factors
Administer lactulose
Administer neomycin, which is used to kill bacteria in the gut that produces ammonia , complication of this medication is vitamin K deficiency. This bacteria in the gut help produce folic acid,riboflavin, and vitamin K.
Adjust doses of medication that are metabolized by the liver
Monitor your glucose
Administer mucomyst for suspected Tylenol or
Perform a Neuro assessment
Transjugular intrahepatic portosystemic shunt tips procedure -a stent is inserted, allowing the shunt of blood directly from the hepatic veins into the portal veins, bypassing the liver which decreases the portal hypertension. This is a procedure for select patients to relieve esophageal disease or ascites.
Spleen
A person with a history of splenectomy has reduced immune function since the spleen is thought to filter the blood.
Signs of a splenic rupture includes sharp, left shoulder pain, which is also known as kehr’s sign (diaphragmatic irritation causes referred pain)
abdominal distention with absent bowel sounds
Abdominal trauma clinical signs
ECCHYMOSIS over left upper quadrant-soft tissue trauma or splenic injury
Ecchymosis around umbilicus-cullen’s sign-intraperitoneal bleeding
Ecchymosis of the flank -grey turner’s sign-RETROPERITONEAL bleeding
Left shoulder pain (kehr’s sign)-ruptured spleen
Absence of bowel sounds with Abd distention and guarding -visceral injury
Bowel sounds in chest-diaphrgamatic rupture
Free air in Abd confirmed by x ray-disruption of the GI tract
Diagnostic peritoneal LAVAGE positive for blood- intra Abd bleeding
Intra-Abd hypertension and abdominal compartment syndrome
Etiology-massive fluid resuscitation, trauma, emergent Abd surgery
Pathophysiology-if pressure in the abdominal cavity becomes greater than the pressure in the capillaries that perfuse the abdominal organs, ischemia but makes absolutely no sense that she said she live her life and infarction may result. It may also result in reduce cardiac output, increase systemic vascular resistance, reduce venous return and decrease renal perfusion.
Intra-abdominal hypertension= if it is over 12-15mmhg
Abd perfusion pressure-the difference between map and iap
App 60 and over is associated with improved survival
App 50 and under is associated with mortality
Measure the bladder pressure, place transducer at the level of the symphysis pubis to get an accurate pressure
If over 2pm he, then laparotomy should be considered
Intra-Abd hypertension and abdominal compartment syndrome Treatment
For IAP of 12 or greater-
Loosen constrictive clothing
Manage pain and agitation
Prevent overhydration
Place a NG tube to lis to decompress the abdomen
Optimize stool management, assess for impaction
Discuss with physician whether gastro/colon prokinetic agents are appropriate pt
Optimize patient position in reverse trendelenburg and maintaining head of bed at 20 degrees or less
For iap over 20-
This is Abd compartment syndrome
Decompression surgery may be indicated
