Gastrointestinal Bleeding - NCM 118 Medical Surgical Nursing - ILOILO DOCTORS’ COLLEGE PDF

MEDICAL SURGICAL NURSING 1 ST semester ILOILO DOCTORS’ COLLEGE ACADEMIC YEAR BACHELOR OF SCIENCE IN NURSING...

MEDICAL SURGICAL NURSING 1 ST semester ILOILO DOCTORS’ COLLEGE ACADEMIC YEAR BACHELOR OF SCIENCE IN NURSING 2024 – 2025 Age: GASTROINTESTINAL BLEEDING Morbidity and mortality rates increased with age; 73.2% of deaths occurred in patients older than 60 years ▪ Internal bleeding in the digestive tract Anatomy ▪ Gastrointestinal bleeding can occur anywhere within the gastrointestinal tract UGIB arises from branches of the: o celiac artery and This includes: o superior mesenteric artery (SMA) the esophagus leading to the stomach The patient history findings include: the stomach itself and Weakness the intestines Dizziness Syncope associated with: BACKGROUND o Hematemesis (coffee ground vomitus) Infections (disease) some medicines (drugs) and alcohol o Melena (black stools with rotten odor o Hematochezia (red or maroon stool) can damage tissue in the GI tract and produce bleeding Clinical Presentation: History The diagnosis and therapy for gastrointestinal bleeding (GIB) has evolved over the past 3 decades: Patients may have a history of previous: o dyspepsia (especially nocturnal symptoms) ► peptic from passive diagnostic esophagogastroduodenoscopy ulcer disease with medical therapy o Early satiety to active intervention with endoscopic techniques followed by: o Nonsteroidal anti-inflammatory drug or aspirin use angiographic and surgical approaches if endoscopic therapy failed Many patients with UGIB who are taking nonsteroidal anti- inflammatory drugs present without dyspepsia but with: Gastrointestinal (GI) bleeding are classified into: upper or lower o hematemesis or melena as their first symptom depending on their location in the GI tract Low-dose aspirin (81 mg) has been associated with UGIB UPPER GASTROINTESTINAL BLEEDING: Patients with a prior history of ulcers are at an especially Upper GI bleeding originates in the first part of the GI tract: increased risk for UGIB when placed on: the esophagus, stomach, or duodenum (first part of the intestine) o aspirin or NSAID therapy and should receive LOWER GASTROINTESTINAL BLEEDING: continuous acid suppression with a PPI Lower GI bleeding originates in the portions of the GI tract farther Because recurrence of ulcer disease is common, history findings are down the digestive system: relevant: o the segment of the small intestine farther from the stomach, o Patients may present in a more subacute phase with a large intestine, rectum, and anus history of dyspepsia and occult intestinal bleeding manifesting as a positive fecal occult blood UPPER GASTROINTESTINAL BLEEDING test result or as iron deficiency anemia (UGIB) A history of recent aspirin ingestion suggests that the patient may Upper gastrointestinal (GI) bleeding (UGIB) is defined as hemorrhage have nonsteroidal anti-inflammatory drug gastropathy with an that emanates proximal to the ligament of Treitz. enhanced bleeding diathesis from poor platelet adhesiveness. It is a common and potentially life-threatening condition A history of chronic: o alcohol use of more than 50 g/d or More than 350, 000 hospital admissions are attributable to UGIB, o hepatitis (B or C) which has an overall mortality rate of 10% increases the risk of: Although more than 75% of cases of bleeding cease with supportive o variceal hemorrhage measures, a significant percentage of patients require further o gastric antral vascular ectasia (GAVE) or intervention, which often involves the combined efforts of: o portal gastropathy o gastroenterologists o surgeons and o interventional radiologist The presence of postural hypotension indicates: o more rapid and Race: o severe blood loss No well-described racial predilection for UGIB exists Physical Examination Sex: The goal of the patient's physical examination is to evaluate for: The male-to-female ratio is approximately 2:1 in both countries o shock ****The mortality rates are similar in both sexes o blood loss SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Pulse and blood pressure should be checked with the patient in: The color of stool containing blood depends on the transit o supine and time o upright positions Rapid transit from the upper gastrointestinal tract can result to note the effect of blood loss in red or maroon stools Melena results from more than 100 mL of blood with Significant changes in vital signs with postural changes indicate ► an moderate transit time acute blood loss of approximately 20% or more Slow transit of blood from the lower intestine can result in melena in the presence of obstruction Other signs of shock include: o extremities: cool, pale and often cyanotic Remember 4: o Skin: grayish, moist, diaphoresis Urgent endoscopy is indicated when patients present with: o Oliguria o hematemesis o chest pain, dyspnea o melena or o Tachypnea o postural changes in blood pressure o presyncope: lethargy, somnolence, confusion, and delirium Other signs of shock include: Remember 5: o Peripheral pulses are weak and typically rapid Primary surgical intervention should be considered in o BP < 90 mmHg patients with a perforated viscus from: o duodenal ulcer Hematemesis and melena should be noted o gastric ulcer or The redder the stool ► the more rapid the transit, ►which o Boerhaave syndrome suggests a large upper tract hemorrhage Remember 6: Signs of chronic liver disease should be noted, including: In patients who are poor operative candidates: o spider angiomata o conservative treatment with nasogastric suction o gynecomastia o and broad-spectrum antibiotics can be instituted o splenomegaly o Endoscopic clipping or sewing techniques have also been o ascites used in such patients o pedal edema and o asterixis Differentials Diagnosis 1) Duodenum, Ulcers Signs of tumor are uncommon but portend a poor prognosis 2) Esophagus: Tear , Varices, Cancer, Esophagitis, Boerhaave Signs include: syndrome o nodular liver 3) Gastric: Carcinoma, Ulcer, Gastritis o abdominal mass 4) Portal Hypertension o enlarged and firm lymph nodes Lab-workup The finding of subcutaneous emphysema with a history of vomiting is CBC with platelet count. suggestive of Boerhaave syndrome (esophageal perforation) and requires prompt consideration of surgical therapy Basic metabolic profile (BMP): o BUN UGIB CAUSES o Creatinine o Electrolytes The major causes of UGIB are: o Glucose level o duodenal ulcer hemorrhage (25%) o Fluid balance o gastric ulcer hemorrhage (20%) o mucosal tears of the esophagus or fundus (Mallory-Weiss tear) Lab-workup o esophageal varices o Coagulation parameter: PT, aPPT o erosive gastritis o erosive esophagitis Liver profile: The liver profile can identify: o Dieulafoy lesion o hepatic comorbidity and o gastric varices o suggest underlying liver disease o gastric cancer and o ulcerated gastric leiomyoma Lab-workup Calcium level: Rare Causes A calcium level is useful to identify the patient with: o aortoenteric fistula o hyperparathyroidism o gastric antral vascular ectasia o as well as to monitor calcium in patients receiving multiple o angiectasias and transfusions of citrated blood o Osler-Weber-Rendu syndrome Lab-workup Remember 1: Gastrin level: The proportion of UGIB cases caused by peptic ulcer disease A gastrin level can identify the rare patient with gastrinoma as the has declined cause of: This decline is believed to be due to the use of: PPIs and H pylori o UGIB and therapy o multiple ulcers Patients should be considered for upper endoscopy if blood loss from the upper gastrointestinal tract is suspected Imaging Studies Chest radiographs should be ordered to exclude: Remember 2: o aspiration pneumonia A high level of suspicion of UGIB should exist when the patient o effusion has a history of intake of aspirin or NSAID, even if no history of: o esophageal perforation hematemesis or melena exists Remember 3: c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Upright films should be ordered to exclude perforated viscus and ETIOLOGY AND RISK FACTORS ileus Leading causes: Barium contrast studies are not usually helpful and can make Motor-vehicle accidents endoscopic procedures more difficult (i.e. white barium obscuring Assaults the view) Falls Angiography may be useful if: Sports-related trauma o bleeding persists and endoscopy fails to identify a bleeding site CT scan and ultrasonography may be indicated to evaluate: MECHANISMS OF INJURY o liver disease with cirrhosis Head injuries are caused by a sudden impact force to the head or o cholecystitis with hemorrhage inertial forces within the skull o pancreatitis with pseudocyst and hemorrhage aortoenteric Three Major Mechanisms of Injury: fistula Penetrating injury o other unusual causes of upper gastrointestinal hemorrhage An ECG should be ordered to exclude: Diffuse Injuries such as a blow to the skull o arrhythmia Rebound of the cranial contents may result in an area of o acute myocardial infarction- due to hypotension injury opposite the point of impact Performing a troponin test may be useful to identify patients with: o severe coronary ischemia o atypical myocardial infarction Procedures Nasogastric lavage (1): This procedure may confirm recent bleeding (coffee ground appearance). Possible active bleeding (red blood in the aspirate that does not clear) Nasogastric lavage (2): A nasogastric tube is an important diagnostic tool, and tube placement can reduce the patient's need to vomit. Placement for diagnostic purposes is not contraindicated in patients with possible esophageal varices Treatment Medical Care Surgical Care OTHER MECHANISMS: Medical Care Penetrating trauma- a form of primary injury and includes the The goal of medical therapy is to correct: shock coagulation head wounds made by foreign bodies and by bone fragments abnormalities and to stabilize the patient so that further from skull fracture evaluation and treatment can proceed Coup-countercoup Injuries- term used for complex head injury Stabilize the patient with intravenous fluids: “coup”- French word which means blow o usually normal saline: except in patients with severe Scalp injuries- can cause lacerations, hematomas, and liver disease, ascites, or heart failure contusions and abrasions o and transfuse to maintain a hemoglobin level of 8-10 g Skull fracture- often caused by a force of sufficient to fracture the o Promptly correct any abnormalities in coagulation skull and cause brain injury o Early aggressive resuscitation can reduce mortality in acute UGIB THREE TYPES OF SKULLS FRACTURE Surgical Care Linear Skull Fracture- appear as thin lines Endoscopic on X-ray and does not require treatment Celiotomy Depressed Skull Fracture- maybe palpated and are seen on x-ray Consultations Basilar skull fracture- occurs in bones over Consultation with a surgeon should be considered for all the base of the frontal and temporal lobes patients with gastrointestinal hemorrhage manifested as ecchymosis around the eyes and behind the ears or by blood or CSF leakage from the ear TRAUMATIC BRAIN INJURY BRAIN INJURIES An insult to the brain that is capable of producing intellectual, A. Concussions- head trauma resulting from a blow emotional, social and vocational changes B. Contusion- the brain itself is injured or damaged C. Diffused axonal injury- most severe form of head injury 30 % of cases are fatal because there is no focal lesion to remove 20 % die of secondary brain injury o -involves entire tissue of the brain and occurs at the microscopic level SECONDAY BRAIN INJURY includes: Ischemia from hypoxia and hypotension TYPES OF DIFFUSED AXONAL INJURY Secondary hemorrhage and; Mild- Loss of consciousness and 6-24 hours, short term disability Cerebral edema Moderate- coma lasting less than 24 hours with incomplete recovery on awakening Severe involves primary injury to the brain stem. c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) FOCAL INJURIES Epidural hematoma (extradural hematoma)- forms between the SURGICAL MANANGEMENT skull and the dura matter Removal of epidural clot by craniotomy Subdural hematoma- collection of blood in the subdural space Debridement for penetrating wounds Intracerebral hematoma- occurs less often than epidural in subdural hematomas NURSING MANAGEMENT o caused by bleeding directly into the brain tissue Assessment o Level of Consciousness o Vital signs o Neurovital Signs Maintaining nutrition Monitoring intake and output COMMON NURSING DIAGNOSIS Risk for ineffective airway clearance Ineffective cerebral tissue perfusion Disturbed thought process SIRS AND MODS (organ failure) PATHOPHYSIOLOGY SIRS Kinetic energy transmitted to the brain Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults Rapid brain tissue displacement Generalized inflammation in organs remote from the initial insult Disruption of Blood vessels TRIGGERS o Mechanical tissue trauma: burns, crush injuries, surgical Bleeding procedures o Abscess formation: intraabdominal, extremities Tissue injury due to hypoxia o Ischemic or necrotic tissue: pancreatitis, vascular disease, myocardial infarction Edema o Microbial invasion: bacteria, viruses, fungi o Endotoxin release: gram-negative bacteria CLINICAL MANIFESTATIONS o Global perfusion deficits: post–cardiac resuscitation, shock states Skull Fracture o Regional perfusion deficits: distal perfusion deficits CSF and other fluid drainage from the ear or nose Evidence of various nerve injuries MODS Blood behind the tympanic membrane Multiple organ dysfunction syndrome (MODS) is the failure of Raccoon eyes two or more organ systems. Battle’s sign o Homeostasis cannot be maintained without intervention. Cranial Nerve and Inner Ear damage o Results from SIRS Visual Changes o Mortality rates are linearly related to the number of failed Hearing loss /disturbances organ systems Anosmia Stage 1 Dilated pupils Increased volume requirements Facial paresis or paralysis Mild respiratory alkalosis which is accompanied by oliguria, Vertigo hyperglycemia and insulin requirements. Nystagmus Stage 2 Tachypneic, hypocapnic and hypoxemic. DIAGNOSTIC PROCEDURES Moderate liver dysfunction Physical Exam Possible hematologic abnormalities. History Skull X-ray Stage 3 Shock with BUN/creatine, acid-base disturbances. MRI Significant coagulation abnormalities. CT-Scan Glasgow Coma Scale Stage 4 Vasopressor dependent and UO. MEDICAL MANAGEMENT Ischemic colitis and lactic acidosis follow. Management focuses on supporting all organ functions Ventilatory support Management of fluid balance and elimination Management of nutrition and gastrointestinal function Lab tests Lowering ICP c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Cardiovascular system Myocardial depression and massive vasodilation Neurologic system Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion Often early sign of MODS Renal system Acute renal failure Hypo-perfusion Release of mediators Activation of renin-angiotensin- aldosterone system Nephrotoxic drugs, especially antibiotics GI system Motility decreased: abdominal distention and paralytic ileus Decreased perfusion: risk for ulceration and GI bleeding Potential for bacterial translocation Hypermetabolic state Hyperglycemia-hypoglycemia Insulin resistance Catabolic state Liver dysfunction Lactic acidosis Hematologic system DIC Electrolyte imbalances Metabolic acidosis SIRS AND MODS COLLABORATIVE CARE Prognosis for MODS is poor. Goal: prevent the progression of SIRS to MODS Vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction are critical. PREVENTION AND TREATMENT OF INFECTION PATHOPHYSIOLOGY Aggressive infection control strategies to decrease risk for SIRS AND MODS nosocomial infection Consequences of inflammatory response Once an infection is suspected, institute interventions to control Release of mediators the source. Direct damage to the endothelium MAINTENANCE OF TISSUE OXYGENATION Hypermetabolism Decreased O2 demand Vasodilation leading to decreased SVR Sedation Increase in vascular permeability Mechanical ventilation Activation of coagulation cascade Paralysis Organ and metabolic dysfunction Analgesia Hypotension NUTRITIONAL AND METABOLIC NEEDS Decreased perfusion Goal of nutritional support: preserve organ function Formation of microemboli Total energy expenditure is often increased 1.5 to 2.0 times. Redistribution or shunting of blood Use of the enteral route is preferred to parenteral nutrition. Respiratory system Monitor plasma transferrin and prealbumin levels to assess Alveolar edema hepatic protein synthesis. Decrease in surfactant Increase in shunt V/Q mismatch End result: ARDS c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Obstructive Uropathy SUPPORT OF FAILING ORGANS ARDS: aggressive O2 therapy and mechanical ventilation DIC: appropriate blood products CLINICAL COURSE Renal failure: continuous renal replacement therapy or dialysis ONSET: begins when the kidney is injured and lasts from hours to days. SIRS AND MODS NURSING MANAGEMENT OLIGURIC-ANURIC PHASE: (urine volume less than 400 to 500 mL /24 hours). Reduce chance of infection Dressing changes on all invasive line sites and surgical a. Accompanied by rise in serum concentration of elements wounds according to protocol usually excreted by kidney (urea, creatinine, organic acids, Maintain aseptic technique with all dressing changes and and intracellular cations- potassium and magnesium). manipulation of intravenous lines. b. b. There can be a decrease in renal function with increasing nitrogen retention even when the patient is excreting more Institute the measures that are necessary to prevent than 2-3 L of urine daily- called aspiration when patients are placed on enteral feedings. non-oliguric or high-output renal failure. Keep the head of the bed elevated, and check for residual volume and tube placement every 4 hours DIURETIC PHASE: begins when the 24-hour urine volume exceeds Oral care if on ventilator 500 mL and ends when the BUN and serum creatinine levels stop rising. Provide frequent rest periods Create a quiet environment whenever possible. RECOVERY PHASE: Schedule procedures and nursing care interventions so that c. Usually lasts several months to 1 year. the patient has periods of uninterrupted rest. d. Probably some scar tissue remains, but the functional loss is Manage situations of increased metabolic demand— such not always clinically significant. as fever, agitation, alcohol withdrawal, and pain—promptly so that the patient conserves energy and limits oxygen CLINICAL MANIFESTATION consumption. Monitor bony prominences and areas of high risk for skin 1.Prerenal breakdown. Decreased tissue turgor Dryness of mucous membranes ACUTE RENAL FAILURE Weight loss a syndrome of varying causation that results in a sudden decline in Hypotension renal function. It is frequently associated with an increase in BUN and Oliguria or anuria creatinine, oliguria (less than 500 mL urine/24 hours), hyperkalemia, Flat neck veins and sodium retention. Tachycardia Results in retention of toxins, fluids, 2.Intrarenal and end products of metabolism Edema usually present Usually reversible with medical treatment. 3.Postrenal also called Acute Kidney injury Obstruction to urine flow Obstructive symptoms of BPH (Benign Prostatic Hyperplasia or Hypertrophy) Possible nephrolithiasis 4. Changes in urine volume and serum concentrations of BUN, ETIOLOGY creatinine, potassium Prerenal- result from conditions that decrease renal blood flow Subjective symptoms such as: Nausea Hypovolemia, shock, blood loss, embolism, burns, cardiovascular disorders, sepsis Loss of appetite Intrarenal – result from injury to renal tissue and are usually Headache associated with: Lethargy Nephrotoxic agents, infections, ischemia and Tingling in extremities blockages, polycystic kidney disease Postrenal- arise from obstruction or disruption to urine flow anywhere along the urinary tract. Stones, blood clots, BPH, urethral edema from invasive procedures OTHER MAJOR CAUSES: Vascular Disease Glomerular Disease Interstitial/Tubular Disease c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) DIAGNOSTIC EVALUATION Urinalysis- reveals proteinuria, hematuria, casts Rising serum creatinine and BUN levels Urine chemistry examinations to distinguish various forms of acute renal failure; decreased sodium Renal Ultrasonography- for estimate of renal size and to exclude a treatable obstructive uropathy PATHOPHYSIOLOGY NURSING ASSESSMENT 1. Determine if there is a history of cardiac disease, malignancy, sepsis, or intercurrent illness. 2. Determine if patient has been exposed to potentially nephrotoxic drugs (antibiotic, NSAIDs, contrast agents, solvents). 3. Conduct ongoing physical examination for tissue turgor, pallor, alteration in mucous membranes, blood pressure, heart rate changes, pulmonary edema, and peripheral edema. 4. Monitor intake and output. NURSING DIAGNOSES Excessive Fluid Volume related to decreased glomerular filtration rate and sodium retention Risk for infection related to alterations in immune system and host defenses Imbalanced Nutrition: Less Than Body Requirements related to catabolic state, anorexia, and malnutrition associated with acute renal failure. Risk for Injury related to GI Bleeding Disturbed Thought Processes related to the effects of uremic toxins on the central nervous system(CNS). MEDICAL MANAGEMENT Fluid and dietary restrictions Maintain Electrolytes May need dialysis to jump start renal function May need to stimulate production of urine with IV fluids, Dopamine, diuretics, etc. MANAGEMENT: Preventive Measures 1. Identify patients with preexisting renal disease. 2. Initiate adequate hydration before, during, and after any procedure requiring NPO status. 3. Avoid exposure to nephrotoxins. Be aware that the majority of drugs or their metabolites are excreted by the kidneys. *DRUG ALERT: Nonsteroidal anti-inflammatory drugs (NSAID’s) including COX-2 inhibitors, may reduce glomerular filtration rate in people at risk for renal insufficiency, causing renal failure. c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) 4. Monitor chronic analgesic use-some drugs may cause interstitial PREVENTING GI BLEEDING nephritis and papillary necrosis. ✓ Examine all stools and emesis for gross and occult blood. 5. Prevent and treat shock with blood and fluid replacement. Prevent ✓ Administer H2-receptor antagonist, such as cemetidine (Tegamet) long periods of hypotension. or ranitidine (Zantac), or nonaluminum or magnesium antacids as 6. Monitor urinary output and CVP hourly in critically ill patients to prophylaxis for gastric stress ulcers. detect onset of renal failure at the earliest moment. 7. Schedule diagnostic studies requiring dehydration so there are “rest ✓ Prepare for endoscopy when GI bleeding occurs. days”, especially in aged who may not have adequate renal reserve. PRESERVING NEUROLOGIC FUNCTION 8. Pay special attention to draining wounds, burns, which can lead to dehydration and sepsis and progressive renal damage. ✓ Speak to the patient in simple orienting statements, using 9. Avoid infection; give meticulous care to patients with indwelling repetition when necessary. catheter or I.V.lines. ✓ Maintain predictable routine, and keep change to a minimum. ✓ Watch for and report mental status changes-somnolence, MANAGEMENT: lassitude, lethargy, and fatigue progressing to irritability, Corrective and Supportive Measures disorientation, twitching, seizures. Corrective reversible cause of acute renal failure (e.g, improve ✓ Correct cognitive distortions. renal perfusion, maximize cardiac output, surgical relief of ✓ Use seizure precautions-padded side rails, airway and suction obstruction). equipment at bedside. Be alert for and correct underlying fluid excesses or deficits ✓ Encourage and assist patient to turn and move because Correct and control biochemical imbalances-treatment of drowsiness and lethargy may prevent activity. hyperkalemia. ✓ Use music tapes to promote relaxation. Restore and maintain blood pressure. Maintain nutrition. MANAGEMENT OF LOWER GI BLEED COMPLICATIONS: Infection Lower gastrointestinal bleeding is blood loss from the gastrointestinal Arrhythmias due to hyperkalemia tract of recent onset emanating from a location distal to the ligament of Treitz resulting in instability of vital signs, anemia, and/or need for Electrolyte (sodium, potassium, calcium, phosphorus) blood transfusion. abnormalities GI Bleeding due to stress ulcers Multiple organ systems failure ETIOLOGY NURSING INTERVENTIONS ACHIEVING FLUID AND ELECTROLYTE BALANCE ✓ Monitor for signs and symptoms of hypovolemia or hypervolemia ✓ Monitor urinary output and urine specific gravity; measure and record intake and output including urine, gastric suction, stools, wound drainage, perspiration. ✓ Monitor serum and urine specific concentrations. ✓ Weigh patient daily to provide an index of fluid balance; expected weight loss is ½ to 1 Ib (0.25- 0.5 kg) daily. ✓ Adjust fluid intake to avoid volume overload and dehydration. ✓ Evaluate for signs and symptoms of hyperkalemia and monitor Diverticular diseases(MC) – in elderly males. serum potassium levels. Angiodysplasia ✓ (Notify health care provider of value above 5.5mg/L) ✓ Watch for cardiac arrhythmia and heart failure from hyperkalemia, Anorectal diseases – in middle aged males. electrolyte imbalance, or fluid overload. Have resuscitation Carcinoma/polyps equipment on hand in case of cardiac arrest. Colitis – ischemic, infective, radiation ✓ Instruct patient about the importance of following prescribed diet, avoiding foods high in potassium. Inflammatory bowel disease (IBD) ✓ Administer blood transfusions during dialysis to prevent Meckel`s diverticulum – in childhood hyperkalemia from stored blood. Uncommon causes PREVENTING INFECTION Varices (Rectal) ✓ Monitor for all signs of infection. Be aware that renal failure Intussusception patients do not always demonstrate fever and leukocytosis. ✓ Remove bladder catheter as soon as possible; monitor for UTI. Solitary rectal ulcer ✓ If antibiotics are administered, care must be taken to adjust the Aorto enteric fistulae dosage for renal impairment. Vasculitis NSAID induced ulcer, colitis MAINTAINING ADEQUATE NUTRITION ✓ Work collaboratively with dietitian to regulate protein intake Small intestinal causes according to impaired renal function. ✓ Offer high carbohydrate feedings because carbohydrates have a Vascular ectasias greater protein-sparing power and provide additional calories. Tumors ✓ Weigh daily ✓ Be aware that food and fluids containing large amounts of UPPER GI SOURCE should always be excluded in all patients with potassium, sodium, and phosphorus may need to be restricted. massive lower GI bleeding. c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) SIGNS AND SYMPTOMS LOCALIZATION OF THE BLEEDING SITE The clinical presentation of LGIB varies with the anatomical source of In about 10% of patients presenting with LGIB, the source of the bleeding, as follows: bleeding is from the upper gastrointestinal (GI) tract. Maroon stools, with LGIB from the right side of the colon Some patients with LGIB should have a nasogastric (NG) tube Bright red blood per rectum with LGIB from the left side of placed, and if the aspirate or lavage does not show any blood or the colon coffee ground–appearing material but dose show bile, bleeding originating from the upper GI tract is unlikely. Melena with cecal bleeding In case of high suspicion, obtain an However, patients with upper GI bleeding and right-sided colonic esophagogastroduodenoscopy (EGD) evaluation bleeding may also present with bright red blood per rectum if the bleeding is brisk and massive. INITIAL APPROACH TO HEMOSTASIS The presentation of LGIB can also vary depending on the etiology. A In patients who are hemodynamically stable with mild to moderate young patient with infectious or noninfectious (idiopathic) colitis may bleeding or in patients who have had a massive bleed that has present with the following: stabilized, colonoscopy should be performed initially. Once the Fever bleeding site is localized, therapeutic options include coagulation Dehydration and injection with vasoconstrictors or sclerosing agents. Abdominal cramps For diverticular bleeding, bipolar probe coagulation, epinephrine injection, and metallic clips may be used. If recurrent bleeding is Hematochezia present, the affected bowel segment can be resected. For angiodysplasia, thermal therapy, such as electrocoagulation APPROACH CONSIDERATION or argon plasma coagulation, is generally successful. Angiodysplastic lesions may be missed at colonoscopy if the The management of LGIB has 3 components, as follows: lesions are small or covered with blood clots. Resuscitation and initial assessment The 2008 SIGN guideline states that colonoscopic hemostasis is Localization of the bleeding site an effective way to control hemorrhage from active diverticular or Therapeutic intervention to stop bleeding at the site post-polypectomy bleeding in patients with massive LGIB. RESUSCITATION AND INITIAL ASSESSMENT THERAPEUTIC INTERVENTION Initial resuscitation involves establishing large-bore IV access and Therapeutic intervention to stop bleeding at the site includes: administration of normal saline. Besides ordering routine Colonoscopy laboratory studies (eg, complete blood cell (CBC) count, Vasoconstrictive Therapy electrolyte levels, and coagulation studies), blood should be typed and cross-matched. Superselective Embolization Endoscopic therapies The 2008 SIGN guideline states that patients in shock should Emergent surgery receive fluid volume replacement without delay. Colloid or crystalloid solutions may be used to achieve volume restoration COLONOSCOPY before administering blood products. Red cell transfusion should Colonoscopy is useful in radiation therapy–induced be considered after loss of 30% of the circulating volume. gastrointestinal (GI) bleeding and in the treatment of colonic polyp lesions. Signs of hemodynamic compromise include postural changes with dyspnea, tachypnea, and tachycardia. Endoscopic treatment of radiation-induced bleeding includes topical application of formalin, Nd:YAG laser therapy, and argon An orthostatic drop in systolic blood pressure of more than 10 mm plasma coagulation. Hg or an increase in heart rate of more than 10 beats per minute Neoplastic bleeding due to polyps requires polypectomy. is indicative of at least 15% of blood volume loss. Patients diagnosed with colonic tumors may require surgical resection. Severe postural dizziness with a postural pulse increase of at least 30 beats per minute is a sensitive and specific indicator of VASOCONSTRICTIVE THERAPY acute blood loss of more than 630 mL. In patients in whom the bleeding site cannot be determined based on colonoscopy and in patients with active, brisk LGIB, Coagulopathy, such as an international normalized ratio (INR) of angiography with or without a preceding radionuclide scan should greater than 1.5, may require correction with fresh frozen plasma; be performed to locate the bleeding site as well as to intervene thrombocytopenia can be corrected with platelet transfusions. therapeutically. Transfer to ICU Initially, vasoconstrictive agents, such as vasopressin can be Patients who require admission to the intensive care unit and used. early involvement of both a gastroenterologist and a surgeon An experimental study of treatment of LGIB by selective arterial include the following: infusion of vasoconstrictors, such as epinephrine with propranolol Patients in shock and vasopressin, was reported. Although epinephrine and Patients with continuous active bleeding propranolol drastically reduced mesenteric blood flow, they also Patients at high risk, such as patients with serious comorbidities, caused a rebound increase in blood flow and recurrent bleeding. those needing multiple blood transfusions, or those with an acute Vasopressin is a pituitary hormone that causes severe abdomen vasoconstriction in the splanchnic bed. Vasoconstriction reduces the blood flow and facilitates hemostatic plug formation in the bleeding vessel. Vasopressin infusions are more effective in diverticular bleeding, which is arterial, as opposed to angiodysplastic c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) bleeding, which is of the venocapillary type. The results are Rossetti at al reviewed 11 years of experience in less than satisfactory in patients with severe atherosclerosis transarterial embolization of acute colonic bleeding in and coagulopathy. Switzerland. Intra-arterial vasopressin infusions begin at a rate of 0.2 Twenty-four patients underwent colonic embolization for U/min, with repeat angiography performed after 20 minutes. diverticular, post-polypectomy, bleeding, and bleeding from The bleeding stops in about 91% of patients receiving intra- cancer, angiodysplasia, and hemorrhoids. arterial vasopressin but recurs in up to 50% of patients when All bleeding stopped except hemorrhoidal bleeding, requiring the infusion is stopped. hemorrhoidal ligature. If bleeding persists, the rate of the infusion is increased to The risk of bowel ischemia was 21%. 0.4-0.6 U/min. In another study by Yap et al, 95 patients underwent Once the bleeding is controlled, the infusion is continued in embolization for acute GI hemorrhage; 80% of the patients an intensive care setting for 12-48 hours and then tapered had upper GI hemorrhage and the rest had lower GI over the next 24 hours. hemorrhage. In patients with rebleeding, surgery should be considered. Vessels embolized included gastroduodenal (39%), pancreatoduodenal (20%), gastric (19%), superior COMPLICATIONS OF VASOCONSTRICTIVE mesenteric (11%), inferior mesenteric (11%), and splenic artery (4%). THERAPY Immediate hemostasis was obtained in 98% of patients. During vasopressin infusion, monitor patients for recurrent Complications included bowel ischemia in 4% and coil hemorrhage, myocardial ischemia, arrhythmias, migration in 3% of patients. hypertension, and volume overload with hyponatremia. The overall 30-day mortality rate was 18%. Nitroglycerine paste or drip can be used to overcome cardiac complications. Selective mesenteric infusion induces bowel wall contraction COMPLICATIONS OF SUPERSELECTIVE and spasms. EMBOLIZATION Do not administer vasopressin into systemic circulation intravenously, because this causes coronary Rosenkrantz et al reported 3 cases of colonic infarction. vasoconstriction, diminished cardiac output, and One patient died following segmental colectomy, and the tachyphylaxis. other patients revealed full-thickness bowel wall injury in the Vasopressin infusions are contraindicated in patients with resected specimen. severe coronary artery disease and peripheral artery Intestinal ischemia and infarction have also been reported. disease. To prevent this complication, perform embolization beyond the marginal artery as close as possible to the bleeding point SUPERSELECTIVE EMBOLIZATION in the terminal mural arteries. An alternative to vasopressin infusion is embolization with The relevance of surgery after embolization of gastrointestinal and abdominal surgery was also studied in agents such as gelatin sponge, coil springs, polyvinyl 2014. alcohol, and oxidized cellulose. Embolization involves superselective catheterization of the In a retrospective study, a total of 54 patients with 55 bleeding events were identified; only 25 patients (45%) had bleeding vessel to minimize necrosis, the most feared LGIB. complication of ischemic colitis. This therapeutic modality is useful in patients in whom The rebleeding rate was 24% (n=6), and 50% of those with recurrent LGIB required surgery. vasopressin is unsuccessful or contraindicated. Initial experience with embolization suggested that The study revealed a primary clinical embolization success rate of 82%, the rate of early recurrent bleeding (< 30 d) was complications of intestinal infarction were as high as 20%. 18%, and the rate of delayed bleeding (>30 days) was 3.6%. With the advent of superselective catheterization and embolization of the vasa recta, successful embolization has Surgery after embolization was required in 20% of patients (n=11). The investigators concluded that surgery has an been performed without intestinal infarction. important role after successful embolization. Embolization is performed using a 3 French (F) microcatheter placed coaxially through the diagnostic 5F catheter. ENDOSCOPIC THERAPIES The therapeutic catheter is advanced as far as the vasa Advantages of upper or lower endoscopic evaluation is that it recta over a 0.018-inch guidewire so as to decrease the risk provides access to therapy in patients with GI bleeding. of infarction. Endoscopic control of bleeding can be achieved using the thermal Once the bleeding vessel is identified, microcoils are used to modalities or sclerosing agents. Absolute alcohol, morrhuate occlude the bleeding vessel and to achieve hemostasis. sodium, and sodium tetradecyl sulfate can be used for Although microcoils are most commonly used, polyvinyl sclerotherapy of upper and lower GI lesions. alcohol and Gelfoam are also used alone or in conjunction Endoscopic epinephrine injection is commonly used because of with microcoils. its low cost, easy accessibility and low risk of complications. An However, if terminal mural branches of the bleeding vessel additional hemostatic method such as clips or thermoregulation is cannot be catheterized, abort the procedure and immediately needed to prevent subsequent bleeding. perform surgery. Endoscopic thermal modalities such as laser photocoagulation, Kuo et al concluded superselective microcoil embolization electrocoagulation, heater probe can also be used to arrest for the treatment of LGIB is safe and effective. hemorrhage. They reported complete clinical success in 86% of patients Endoscopic control of hemorrhage is suitable for GI polyps and with a rebleeding rate of 14%. Minor ischemic complication cancers, arteriovenous malformations, mucosal lesions, rates were noted as 4.5%, and major ischemic complication postpolypectomy hemorrhage, endometriosis, and colonic and rates were reported as 0%. rectal varices. c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Postpolypectomy hemorrhage can be managed by Formulating and interventional plan electrocoagulation of the polypectomy site bleeding with either Insert a nasogastric (NG) tube in all patients. A clear bile-stained snare or hot biopsy forceps or by epinephrine injection. aspirate generally excludes bleeding proximal to the Treitz Photocoagulation using lasers such as argon laser or Nd:YAG ligamentum. After initial resuscitation, undertake a search for the laser. cause of the bleeding to precisely locate the bleeding point. Argon laser treatment is recommended for mucosal or superficial Following accurate localization by angiogram, bleeding can be lesions, because the energy penetrates only 1 mm. Nd:YAG temporarily controlled with either angiographic embolization or lasers are more useful for deeper lesions, because they penetrate vasopressin infusion to stabilize the patient in anticipation of semi- 3-4 mm. urgent segmental bowel resection Endoscopic therapy for LGIB is a minimally invasive. Segmental bowel resection is performed in the next 24-48 hours following correction of the patient's physiologic parameters, which include hypotension, hypothermia, acute hemorrhagic anemia, EMERGENCY SURGERY and deficient coagulation factors. Emergency surgery is required in about 10-25% of patients with Use selective mesenteric embolization in high-risk patients for lower gastrointestinal bleeding (LGIB) in whom non-operative whom the operative management is associated with prohibitive management is unsuccessful or unavailable. risk of morbidity and mortality. If mesenteric embolization is used, these patients must be carefully monitored for bowel ischemia Surgical indications: and perforation. Any evidence of ongoing bowel ischemia and/or Persistent hemodynamic instability with active bleeding unexplained sepsis following mesenteric embolization requires exploratory laparotomy to resect the affected bowel segment. Persistent, recurrent bleeding Perform subtotal colectomy with ileoproctostomy in patients with Transfusion of more than 4 units packed red bloods cells in a multiple episodes of non-localized LGIB or bilateral sources of 24-hour period, with active or recurrent bleeding colonic hemorrhage. INTRA-OPERATIVE DETAILS SEGMENTAL BOWEL RESECTION AND SUBTOTAL COLECTOMY Surgical intervention is required in only a small percentage of patients with LGIB. The surgical option depends on whether the Segmental bowel resection following precise localization of the bleeding source has been accurately identified preoperatively; if bleeding point is a well-accepted surgical practice in so, it is then possible to perform segmental intestinal resection. hemodynamically stable patients. If the bleeding source is unknown, an upper gastrointestinal The procedure of choice in patients who are actively bleeding endoscopy should be performed before any surgical exploration. from an unknown source. The abdominal cavity is explored through a midline vertical Intraoperative esophagogastroduodenoscopy (EGD), surgeon- incision. The assistance of a gastroenterologist or another guided enteroscopy, and colonoscopy may be helpful in surgical endoscopist or surgeon is required for intraoperative diagnosing undiagnosed massive GI bleeding. endoscopic evaluation. The colonoscope is introduced, and the Patients who are hemodynamically stable should have surgeon assists its passage. On-table colonic lavage and preoperative localization of the bleeding whereas patients who colonoscopy may identify the colonic source of bleeding. are hemodynamically unstable with active bleeding may undergo Surgeon-guided intraoperative small bowel enteroscopy is also emergency exploratory laparotomy with intraoperative endoscopy. performed when no colonic source of bleeding is identified. In patients who are hemodynamically stable, once the bleeding Colonoscopic manipulation of the small bowel may cause site is preoperatively localized, intra-arterial vasopressin is used iatrogenic mucosal tears and hematomas, which may be as a temporizing measure to reduce the bleeding before patients mistakenly identified as a source of bleeding. undergo segmental colectomy. Using this approach the operative Another intraoperative strategy is to clamp segments of the bowel morbidity rate is approximately 8.6%, the mortality rate is around with non-crushing intestinal clamps to identify the segment that 10%, and the rate of rebleed ranges from 0-14%. fills with blood. In patients undergoing emergency laparotomy, every attempt If the bleeding point cannot be diagnosed through intraoperative should be made to localize the bleeding intraoperatively, because pan-intestinal endoscopy and examination, and if evidence points a segmental colectomy is preferred. If the bleeding site is not to a colonic bleeding, perform a subtotal colectomy with end localized, a subtotal colectomy is performed with an inherent ileostomy. morbidity rate of around 37% and a mortality rate of about 11%- 33%. In unstable patients, a two-stage procedure is preferred: POST-OPERATIVE DETAILS temporary end ileostomy and delayed ileoproctostomy. postoperative diarrhea can be a significant problem in elderly Hypotension and shock are the eventual consequences of blood patients who undergo subtotal colectomy and ileoproctostomy. loss, but this depends on the rate of bleeding and the patient's response. PRE-OPERATIVE DETAILS Clinical development of shock may precipitate myocardial infarction, cerebrovascular accident, and renal or hepatic failure. Acute LGIB is a common clinical entity and is associated with Azotemia occurs in patients with gastrointestinal blood loss. significant morbidity and mortality (10-20%). These factors are dependent on the patient age (>60 y), the COMPLICATION OF LOWER GI BLEED presence of multi-organ system disease, transfusion requirements Anemia (>4 units), need for operation, and recent stress (eg, surgery, trauma, sepsis). Shock Kidney failure Complications of blood transfusions 3 major aspects involved in managing LGIB: Complications related to massive blood transfusions (greater Treat shock than one blood volume in 24 hour) are hypothermia, Localization of the source of bleeding hypocalcemia, hyperkalemia, dilutional thrombocytopenia, and coagulation factor deficiencies. c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Chronic kidney disease (CKD) is defined by the presence of kidney COMPLICATION OF SURGERY damage for three or more months and the level of kidney function (National Kidney Foundation [NKF], 2002) The most common early postoperative complications are End stage renal disease (ESRD) represents a clinical state in which intra-abdominal or anastomotic bleeding, there has been an irreversible loss of renal function. mechanical small bowel obstruction (SBO), intra-abdominal sepsis, #CKD often will lead to ERSD localized or generalized peritonitis, Uremia: The presence of excessive amounts of urea in the blood, wound infection and/or dehiscence, which may be a sign of kidney disease or failure. Clostridium difficile colitis deep venous thrombosis (DVT), Azotemia: An elevation of blood urea nitrogen (BUN) and serum creatinine levels. The reference range for BUN is 8-20 mg/dL, and the pulmonary embolus (PE). normal range for serum creatinine is 0.7-1.4 mg/dL. TRANSFUSION FREE MANAGEMENT Glomerular filtration rate (GFR) is the volume of plasma filtered in the glomeruli per unit time, usually reported in mL/min. The management of lower GI bleeding (LGIB) can be challenging in patients who refuse transfusions of blood or blood products. However, transfusion-free management of GI bleeding may be PATHOPHYSIOLOGY effective with an acceptable mortality rate. Studied has been done in Englewood Hospital in which they experience in managing patients with gastrointestinal bleeding who do not accept blood-derived products – most of them survived These results suggest that transfusion-free management of gastrointestinal hemorrhage can be effective with mortality comparable with the general population accepting medically indicated transfusion. Management of these patients is challenging and requires a dedicated multidisciplinary team approach knowledgeable in techniques of blood conservation. Surviving patients were treated with epoetin alfa (Procrit) – stimulate erythropoesis - once daily for 5 days, IV iron dextran(plasa vol expender) infusion once daily for 10 days, IV folic acid daily, vitamin C twice daily, as well as IM vitamin B12 injection once. These patients also received beta-blockers (to reduce the cardiac workload) and supplemental oxygen (100%) with intubation (to improve the oxygen delivery as much as possible without blood transfusions). The overall mortality rate was 10%. LONG TERM MONITORING Postoperative office visits every 2 weeks are essential to ensure proper wound healing. Upon discharge, a general diet abundant in fruits and vegetables is recommended. Patients are instructed to drink 6-8 glasses of fluid per day. Psyllium seed preparationsa(dietary fibre) should also be started. Regardless of the primary cause of nephron loss, some usually Increased levels of physical activity may prevent the progression survive or are less severely damaged of diverticular disease These nephrons then adapt and enlarge, and clearance per Aspirin and NSAID use is associated with increased risk of nephron markedly increases. diverticular bleeding. If the initiating process is diffuse, sudden, and severe, such as in The need for a follow-up colonoscopy is determined by a some patients with rapidly progressive glomerulonephritis recurrence of symptoms. (crescentic glomerulonephritis), acute or subacute renal failure may ensue with the rapid development of ESRD. Angiodysplasia is more likely to rebleed if untreated and may require follow-up intervention to localize and treat recurrent Focal glomerulosclerosis develops in these glomeruli, and they bleeding. eventually become non-functional. Colonoscopic electrocoagulation is generally successful in such At the same time that focal glomerulosclerosis develops, situations. proteinuria markedly increases and systemic hypertension worsens. This process of nephron adaptation has been termed the "final common path." Adapted nephrons enhance the ability of the kidney to postpone uremia, but ultimately the adaptation process leads to the demise CHRONIC KIDNEY DISEASE of these nephrons. c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Adapted nephrons have not only an enhanced GFR but also Family history of kidney disease enhanced tubular functions in terms of, for example, potassium Age 65 or older and proton secretion CLINICAL MANIFESTATION DIAGNOSTIC TESTS 1. Urinalysis: fixed specific gravity 1.010 (low); excess protein, blood cells, cellular casts 2. Urine culture; identify infection 3. BUN and serum creatinine; evaluate kidney function Mild azotemia: BUN 20-50 mg/dl Severe renal impairment: BUN > 100 mg/dl ETIOLOGY Uremic symptoms: > BUN 200mg/dl *Creatinine levels >4 mg/dl = serious renal Diseases and conditions that often lead to CKD include : impairment (**better indicator than BUN of renal Type 1 or type 2 diabetes function); elevated BUN –responsible for neurological symptoms High blood pressure 4. Creatinine clearance: reflects GFR and renal function Glomerulonephritis, an inflammation of the kidney's filtering (most accurate; need 24 hour urine collection) units (glomeruli) 5. *Serum electrolytes: monitored throughout course of CKD Interstitial nephritis, an inflammation of the kidney's tubules 6. CBC: moderately severe anemia with hematocrit 20- and surrounding structures 30%; low hemoglobin; reduced RBC’s and platelets Polycystic kidney disease 7. Renal ultrasonography: CKD; decreased renal size 8. Kidney biopsy: diagnose underlying disease process; Prolonged obstruction of the urinary tract, from conditions differentiate acute from chronic such as enlarged prostate, calculi and some cancers Vesicoureteral reflux, a condition that causes urine to back up into your kidneys MANAGEMENT Recurrent kidney infection, also called pyelonephritis 1. Medications RISK FACTORS General effects of CKD on medication effects Increased half-life and inc. plasma levels of meds excreted Factors that may increase the risk of chronic kidney disease : by kidneys; monitor carefully Diabetes Dosage may change when in renal failure; do not give demerol to patients on dialysis (toxic); digitalis excreted High blood pressure largely by kidney* Heart disease Dec. drug absorption if phosphate-binding agents administered Smoking concurrently Obesity Low plasma protein levels > lead to toxicity when protein- bound drugs are given High cholesterol c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Avoid nephrotoxic drugs (Aminoglycosides, penicillin in high doses, carefully monitor vancomycin due to toxic accumulation); Amphoteracin B very nephrotoxic ; also contrast- CAPD: media induced nephrotoxicity most common *If on dialysis; many drugs removed by dialysis; varies with hemodialysis and peritoneal dialysis: CHECK before serving. continuous ambulatory peritoneal dialysis *Typically do not serve antihypertensive drugs before exchanges 4-5 times a day hemodialysis (BP may drop); give after dialysis. treatments-ongoing 24 hours a day; 7 days a week 2 liters solution in peritoneal cavity except during drain time; independent treatment CCPD: continuous cycler peritoneal dialysis; uses delivery devise (cycler) during nighttime hours and continuous dwell during day 2. Dietary restrictions *Early in CRF: diet modification-slow kidney failure avoid uremic symptoms Restrict proteins (40gm/day) of high biologic value Increase carbohydrate intake (35kcal/kg/day) Limit fluid to 1-2 L per day; limit sodium to 2 g/day (usual guideline is 500-600 ml more than previous’ day’s Kidney Transplant 24 urine output) involves surgically placing a healthy kidney from a donor into Restrict potassium to (60-70 mEg/day; no salt body substitutes); avoid bananas, prunes, raisins, orange can come from deceased or living donors. juice, tomatoes, deep green and yellow vegetables need to take medications for the rest of life to keep body Restrict phosphorus food (especially milk, ice cream, from rejecting the new organ. cheese; also meat, eggs, dairy products) to 1000 mg/day NURSING CARE PLAN 3. Renal replacement therapies *Used when medications and diet are no longer effective ✓ Haemodialysis (AV fistula or graft) ✓ the most common type of dialysis. ✓ During the procedure, a tube is attached to a needle in your arm. Blood passes along the tube and into an external machine that filters it, before it's passed back into the arm along another tube. ✓ usually carried out three days a week, with each session lasting around four hours. 4. Peritoneal dialysis ✓ uses the inside lining of abdomen (the peritoneum) as the filter, rather than a machine. Like the kidneys, the peritoneum contains thousands of tiny blood vessels, making it a useful filtering device. 1. Warmed sterile dialysate instilled into peritoneal cavity via catheter inserted into peritoneal cavity 2. Metabolic waste products and excessive electrolytes diffuse into dialysate while it remains in abdomen 3. Water diffusion controlled by glucose (dextrose) concentration in the dialysate which acts as an “osmotic” agent 4. Amount of solution removed determined by glucose concentration of the dialysate! Excess fluid/solutes removed more gradually; less risk for unstable client 5. Fluid drained by gravity into sterile bag at set interval- removing waste products/ excess fluid Clear” solution ‘fills” abdomen Yellow” urine appearing fluid drains out (looks like urine, should be clear) TYPES OF PERITONEAL DIALYSIS c a l a n t a s p - SCHOOL – COURSE A.Y. 2024 – 2025 MS LEC (NCM 118) Gastrointestinal symptoms (abdominal pain, nausea, vomiting) usually may the first symptom for ESRD patients. Urimic toxins is associated with an unpleasant metallic taste in ESRD patient. Gastritis, peptic disease are common in ESRD patient. DYSLIPIDEMIA A major risk factor for cardiovascular morbidity and mortality, and is very common in CKD. Lipid profiles in CKD patients reflect the level of kidney function and the degree of proteinuria. Prevalence of hyperlipidemia as renal function. o The degree of hypertriglyceridemia and elevation COMPLICATIONS of LDL cholesterol is proportional to severity of renal impairment. LIVER CIRRHOSIS a chronic, degenerative disease characterized by replacement of