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PICU RENAL/GI/ENDO Overview of Anatomy and Physiology The esophagus, stomach, large and small intestine, aided by the liver, gallbladder and pancreas convert the nutritive components of food into energy and break down the non-nutritive components into waste to be excreted. Congenital Acquired 1. Cleft Lip and Cleft Palate GER 2. Pyloric stenosis 3. Biliary atresia Appendicitis 4. Hirschsprung’s disease Celiac disease CCRN FOCUS Acute abdominal trauma Acute GI Hemorrhage Bowel infection/Obstruction/Perforation (nec, mesenteric ischemia, adhesions GER GI Abnormalities (omphalocele, gastrochisis, volvulus, Hirsh. Disease, malrotation, intussusception GI Surgeries Hepatic Failure (portal HTN, cirrhosis, biliary atresia, esophageal varices Malnutrition/malabsorption Hirschsprung Disease Also called congenital aganglionic megacolon Mechanical obstruction from inadequate motility of intestine Incidence: 1 in 5000 live births; more common in males and in Down syndrome Absence of ganglion cells in colon Hirschsprung Disease Clinical Manifestations of Hirschsprung Disease Aganglionic segment usually includes the rectum and proximal colon Accumulation of stool with distention Failure of internal anal sphincter to relax Enterocolitis may occur What to look for? – In a neonate, history commonly reveals a failure to pass meconium and stool within the first 24 to 48 hours after birth. On inspection, the infant may have abdominal distention and easily palpable stool masses. When stool does pass through, its liquid or ribbon like. Diagnostic Evaluation X-ray, barium enema Confirm diagnosis with rectal biopsy Therapeutic Management Surgery Two stages Temporary ostomy Second stage “pull-through” procedure Question Justin, is a 4 month old patient with Trisomy 21 admitted with a new diagnosis of Hirschsprung’s disease. You would expect to see the following on exam…. 1. Jaundice, increased direct bilirubin 2. Foul, ribbon like stools Jaundice increased ammonia 4. Increased PT and PTT followed by hematechezis Intussusception Telescoping or invagination of one portion of intestine into another Intussusception Invagination causes inflammation and swelling at the affected site. Edema eventually causes obstruction and necrosis from occlusion of the blood supply to the bowel http://www.youtube.com/watch?v=Ex6ax VN8TWM What are you looking for? Hx- intermittent attacks of colicky pain characterized by screaming, drawing knees to the chest. Parents report vomitus containing bile or fecal material Jelly like stools Most Common Most common forms include ileocolic (at the ileocecal valve), ileoileal (the ileus into itself), and colocolic (the colon into itself) Intussusception (cont.) Diagnostic evaluation- Spontaneous reduction occurs in up to 10% of patients Therapeutic management- IV fluids, NG decompression- Radiologist guided pneumoenema (air enema) Prognosis – nonoperative reduction is successful in 80% of cases Intussusception (cont.) Nursing considerations- Consent, NPO status, routine labs Why is this problematic? Intestinal perforation/intestinal infarction Intussusception (cont.) Symptoms include acute abdominal pain (manifested in infants by crying and knee chest position, vomiting, and red currant jelly stools. Physical examination may reveal a sausage shaped mass in the right upper quadrant while the lower right quadrant feels empty (dance sign) A barium enema, although often not required, is the test of choice in diagnosing intussusception. The barium enema alone may reduce the intussusception…… Omphalocele herniation of abdominal contents through umbilical ring, usually with an intact peritoneal sac Gastroschisis herniation is lateral to the umbilical ring, and peritoneal sac not present HEPATIC FAILURE Liver Functions Protein synthesis Excretion of metabolic wastes Oxidative phosphorylation Breakdown of glycogen Fatty acid oxidation Synthesis of cholesterol & bile acids Enzymes NADPH Cytochrome P-450 Cytochrome reductase systems Necessities for Normal Liver Function Adequate blood flow Majority of blood flow comes from the portal venous system Oxygen 20 – 40% of cardiac output with only ~25% of blood entering through the Hepatic Artery Hepatocyte damage from hypoxia/hypotension Low-pressure biliary system Biliary Atresia The Biliary organs and duct system that creates, transports, stores, and releases bile into the duodenum for digestion includes the liver, gallbladder, and bile ducts Jaundice, manifesting with yellow discoloration of the kin is the most common early symptom Biliary Atresia—Kasai Procedure MANAGEMENT CONSIDERATIONS Nutrition Gi EN vs. PN Bleed Common Neuro Infection Medications Renal Review of Anatomy/Physiology A- Renal Vein B- Renal Artery C- Ureter D- Medulla E – Pelvis F – Cortex 1 – Ascending limb loop of Henle 2 - Descending limb loop of Henle 3 – Peritubular Capillaries 4 – Proximal Tubule 5 – Glomerulus (Bowman’s capsule + glomerular capillaries) 6 – Distal tubule Clinical Conditions Congenital anomalies of ureter, bladder, urethra Infectious, immunologic, circulatory UTI, Glomerulonephritis, nephrotic syndrome, hemolytic uremic syndrome, CHF Tumors Duplicating systems, strictures, ureterocele, exstrophy of bladder, reflux, hypospadias, Wilm’s tumor Enuresis CCRN FOCUS Acute Renal Failure Chronic Renal Failure Electrolyte Imbalances PHYSIOLOGY: Pediatric Considerations Greater % of total body weight that is water in neonates and infants Immaturity of physiological processes Higher basal metabolic rate and respiratory rate Higher body surface area to weight ratio Health conditions that make children more vulnerable CHLA 2005 PHYSIOLOGY: Metabolic Rate Infant’s adult rate is three times that of an Increased need requires a much higher caloric intake and water requirement. Metabolic turnover of water Infants have 5 times greater turnover of water than adults. Results in increased need for H2O as well as vulnerability to illnesses with dehydration. PHYSIOLOGY: Immature Systems Renal system Matures by 24 months old Decreased Inability GFR to concentrate urine Greater loss daily under normal circumstances Limited renal capabilities until maturity of system is reached FLUID AND ELECTROLYTES Precise regulation is necessary for life Volume and composition remain relatively constant in the presence of wide changes in intake and output Stress and disease increase losses Fluid balance is maintained when excretion and losses are balanced by proper volume and type of fluid intake What is make up of body fluids ?? How do we lose fluid?? PHYSIOLOGY: Total Body Water Premature: 75–80% TBW Newborn: 65-75% TBW One year: 65% TBW Older children: 60% TBW Adolescents: 55-60% TBW PHYSIOLOGY ECF ICF Premature 50% 30% Newborn 50% 30% 1 year 25% 45% Child 20% 45% Adolescent 20% 45% DEHYDRATION: Clinical Management Children’s water requirements in 24 hours 100 ml/kg for first 10 kg 50 ml/kg for next 10 kg 20 ml/kg for each kg above 20 Commercial solutions contain Water, sugar, NA+, K+, CL-, and lactate PEDIALYTE for >12 months old DEHYDRATION: Clinical Management IV fluids when the child is severely dehydrated, usually hospitalized Ringers lactate Isotonic (same osmolarity as blood) Has multiple electrolytes .9 or .45 NS Use after LR to replenish ECF volume Acute Renal Failure Causes: Prerenal: Hypoxia & ischemia due to low blood flow and oxygen delivery Intrarenal: Inflammatory, nephrotoxic, unresolved ischemic flow Postrenal: Obstructive- bladder, ureter, urethra S/S: Electrolyte imbalances, progressive metabolic acidosis Multisystem GI, effects: CNS, dermatologic, CV, respiratory images.MD 2005 Acute Renal Failure Diagnostic Studies: Electrolytes, BUN, creatinine Urinalysis ECG Renal Ultrasound VCUG, etc. Treatment: Prevention is key Diet – high CHO, fats, low protein, sodium, potassium Fluid restriction Careful status, monitoring – electrolytes, fluid Diuretics, antihypertensives, kayexalate, blood products, hemodialysis/peritoneal dialysis Case Scenario Baby Huey 4 mo old Vomiting & Diarrhea x 2 days Wt. 5.6 kg Birth wt: 3.4 kg What information do you want??? History 4 days ago began vomiting and a few loose stools Went to pediatrician – wt in office was 6 kg. Placed on oral rehydration Had fever last night – vomiting continued, brought to ER What other questions would you ask? Physical Assessment Lethargic, dry mucus membranes, dark urine VS: HR 160, RR 48, BP 78/56 Skin turgor – dry Fontanel – sunken What is going on??? What other info do you want??? ENDOCRINE Endocrine system Hypothalamus Pituitary – Anterior, Posterior Thyroid Parathyroid Adrenals – Cortex, Medulla Endocrine Pancreas Testes/ovaries Pineal Hormones Chemical messengers released by endocrine glands Classified by structure, gland of origin or chemical composition Each hormone stimulates a particular receptor in a designated (target) organ or gland The Endocrine System Consists Of Three Components: 1. The cell, which sends a chemical message by means of a hormone 2. The target cells, or end organs, which received the chemical message 3. The environment through which the chemical is transported (blood, lymph, extracellular fluids) from the site of synthesis to the sites of cellular action CCRN ENDOCRINE FOCUS: Acute Hypoglycemia Diabetes insipidus DKA Inborn Errors of Metabolism SIADH Diabetes Mellitus Diabetes (to siphon) Mellitus (honey) Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. (American Diabetes Association Diabetes Care Volume 37, Supplement 1, January 2014) Type 1 Diabetes Autoimmune process-destruction of the pancreatic beta cells. There are multiple genetic markers for predisposition. It is also related to environmental factors. Certain viruses have also been associated with ß-cell destruction. Accounts for only 5-10% of all diabetics but 90-95% of children with diabetes. Presentation Hyperglycemia (high blood sugar) Polyuria (increased urination) Polydipsia (increased thirst) Polyphagia (increased eating) Severity of S/S depends on degree of hyperglycemia and acidosis May appear thin and malnourished May be nauseous or vomiting May be confused or obtunded Intervention Treatment of type 1 diabetes is always insulin and… Blood glucose control Healthy food choices: Avoiding concentrated sweets Carbohydrate counting or consistent carbohydrates Healthy lifestyle: Physical activity Maintain normal weight Hypoglycemia By definition - Blood glucose < 70 mg/dl Symptoms vary. Typically; sweaty, shakiness, tachycardia, and pallor if dropping quickly Behavior change; confusion, irritability, and lack of coordination if lasts longer Can progress to unconsciousness and seizures if untreated Intervention 15 grams of fast acting carbohydrate: 4 oz juice 6 oz regular soda 3-4 tsp honey, sugar, 3-4 candies - should always have something on hand- like glucose tablets, glucose gel Recheck BG in 15 minutes, re-treat till > 70 mg/dl. Follow with snack of protein and carbohydrate if meal not due for 30 minutes. Glucagon IM or SQ - If unconscious or seizing Diabetic Ketoacidosis - DKA Occurs when fat is broken down for energy, due to lack of insulin Fats break down into fatty acids, and glycerol in the fat cells is converted by the liver to Ketones. Eliminated in the urine (ketonuria) or the lungs (acetone breath) Leads to dehydration, acidosis, electrolyte imbalance, coma, and death if untreated Diabetic Ketoacidosis Clinical Manifestations: Hyperglycemia, dehydration, cv collapse Acidosis Hyponatremic Potassium shift ICF to ECF and will eventually decrease Arrhythmia Ketonuria Hyperpnea Mental status changes SIADH Syndrome of Inappropriate Antidiuretic Hormone Low serum osmolality (,275 mOsm/L) Hyponatremic (Na <130mEq/L) Hypervolemic There is increased water reabsorption and vascular volume and decreased urine volume (<0.5ml/kg/hr) SIADH Management includes prevention of complications related to decreased Na+ levels Frequent neuro assessments Hypertonic Loop saline (2-4mL/kg of 3% NSS) diuretics Restrict free water (1/2 to 2/3 of fluid maintenance requirements) DIABETES INSIPIDUS DI is a deficiency of ADH secretion or an insensitivity of renal receptors for uptake of ADH Etiologies include: CNS lesions Lesion or tumor resection Complication Medication of TBI such as Amphotericin B, loop diuretics, some anesthetics (these are reversible) DIABETES INSIPIDUS What to look for: Polyuria, Severe hypernatremia and increased thirst cases lead to hypovolemic shock Management will include: Vasopressin Fluid (SubQ, IV, intranasally DDAVP) replacement 5% dextrose and H2O alternating with D5% with 0.2 NSS) along with maintenance fluids Clinical Manifestations DI SIADH Serum Na+ Increased Decreased Serum osmolality increased Decreased Urine output Increased Decreased Urine Osmolality Decreased Increased Body Weight Stable or decreased Stable or increased BUN Normal or increased Normal or decreased ECF volume Decreased Increased Management Vasopressin, DDAVP, fluid replacement Fluid restriction, Na+ administration for neurologic complications, possibly diuretics Renal Replacement Therapy Peritoneal Dialysis Used for infants and children with ARF or chronic RF Can be ambulatory, manual, or cont. cycling using a device. Dialysate is instilled via catheter. Volume between 15-50 mL/kg K, heparin, and antimicrobials can be added to solution Hemodialysis Used in children with electrolyte imbalance, hypervolemia, pulm. Edema, severe acidosis, anuria, severly elevated BUN & create, CV failure, hepatic failure, hyperammonemia, drug intox. CRRT Used in children with ARF w/ hemodynamic instability, azotemia, sever electrolyte imbalance, hyervolemia, symptomatic metabolic abnormalities. Who are not candidates for PD or HD Renal Replacement Therapy: complications Peritoneal Dialysis Hemodialysis Peritonitis Hypovolemia Catheter issues-leakage, obstruction Hypervolemia Impaired pulm. Function r/t abd. Distention. Filter rupture Systemic bleeding Fluid overload Circuit disconnection Dec. cv output Infection Hypoproteinemia Transfusion rxn. Hyperglycemia r/t absorption of dextrose from solution CRRT Same as HD Dialysis https://youtu.be/fKlY2SKi_dk A 5 year-old female was admitted to ICU following a craniotomy for excision of a tumor. 12 hours post admission the following were noted: Decreased LOC Tacycardia Hypotension Urine output of 15 mL/kg per hour & a SG of 1.003 Na+ 160 Serum osmolality 340 Urine Na+ 20 mmol/d The diagnosis of DI was made. The initial treatment consisted of urine replacement with half NS. 24 hours later her LOC improved, urine output remained at 10-15 mL/kg per hr. with a low SG, serum Na+ 150mmol/L, serum osmolality was 305 mOsm/kg. DDAVP 5mcg/kg intranasally was begun. Within 2 hrs. her urine output had dropped to 3mL/kg hr. with a SG of 1.010. IV replacement of urinary losses was d/c’d and maintenance fluids were continued. Another dose of DDAVP was given for an SG below 1.010 and urine output that exceeded 2mL/kg. 2 days later the IV was d/c’d and DI was managed with BID desmopressin. QUESTION This child would require fluid and electrolyte correction over a period of 48 hours to prevent which of the following? a. Cerebral dehydration & hemorrhage b. Cerebral edema and herniation c. Cerebral hemorrhage and edema d. Cerebral dehydration and herniation QUESTION The cardiovascular signs and symptoms of DI are primarily due to: a. Decreased preload b. Decreased afterload c. Decreased contractility d. Decreased conduction QUESTION Desmopressin is the synthetic form of which of the following? a. ADH b. Renin c. Aldosterone d. Insulin A 6 month old girl has been admitted to the ED with a tempurature of 38.9 and history of cold and flu symptoms for the last 24 hours. She is lethargic, Tachy at 190 bpm, rr is 50/min, bp is 80/45 along with a sunken fontanelle. No wet diapers have been made in the last 18 hours. Which signs and symptoms would indicate dehydration? a. Urine output of less than 0.5mL/kg per hour, decreased urine sodium content, urine osmolality less than 300 b. Urine output < 0.5mL/kg per hour, decreased urine sodium content, urine osmolality > 500 c. Urine output > 1mL/kg per hour, increased urine sodium content, urine osmolality > 500 d. Urine output >1mL/kg per hour, decreased urine sodium content, urine osmolality <300 A child presents to the PICU with lethargy, polyuria, a serum glucose of 550, a blood pH of 7.25, glycosuria, and ketonuria Hyperglycemia is present in the child with uncontrolled DKA due to: A. Decreased tissue utilization of glucose and increased counterregulatory hormones B. Increased counterregulatory hormones and increased tissue utilization of glucose C.Increase tissue utilization of glucose and decreased counterregulatory hormones D. Decreased counterregulatory hormones and decreased tissue use of oxygen Match the laboratory data with symptoms of either SIADH or DI a. Inappropriate secretion of ADH b. hypernatremia c. Low serum sodium and low serum osmolality d. Deficiency of ADH e. Serum hyperosmolality f. Treatment: fluid restriction g. polydipsia h. Treatment: vasopressin or DDAVP i. j. Low urine output in the absence of hypovolemia Dehydration is a complication SIADH: A,C,F,I DI: B,D,E,G,H,J