FLUID & ELECTROLYTES 1.

ACUTE GLOMERULONEPHRITIS - Inflammation of the glomerullar capillaries - Primarily a disease of older children 2 years or at any age CAUSATIVE AGENTS; Group A Beta Hemolytic Streptococcos infection of the throat Infection of the skin Impetigo ( Staphylococcos). Viral, Mumps, Chickenpox, EVB virus, HepB, HIV/AIDS CLINICAL MANIFESTATIONS: -primary presenting features : hematuria (micro/gross, cola-colored urine) Proteinuria Increased BUN and creatinine as urine output decreased Anemia Edema HPN( Hypertension) Flank pain ASSESSMENT & DIAGNOSTIC FINDINGS -Elevated ASO titer: kidneys are swollen, enlarged & congested COMPLICATIONS: -Hypertensive encephalopathy, heart failure, pulmonary edema, End stage renal disease MANAGEMENT: -Treat symptoms, preserve kidney function, treat complications -pharma drugs depend on causative agent: Penicillin for streptococcal infection Steroids for inflammation & edema Diuretics Anti-hypertensive Diet: Decrease dietary protein when BUN is elevated Sodium restriction when with HPN, Edema & heart failure 2. NEPHROTIC SYNDROMES -Primarily a Glumerular disease characterized by: Proteinuria (increased protein in urine)- markedly Hypoalbuminimia Edema Hyperlipidemia (high serum cholesterol & low density lipoprotein) CAUSE: -Any intrinsic renal disease or systemic disease that affects glumerulus (DM) -Generally considered a disease of childhood, may also occur at any age -Causes includes CGN, DM, SLE CLINICAL MANIFESTATIONS: Edema (periorbital, sacrum, ankles,hand, ascitis) Malaise Headache Irritability DIAGNOSTIC FINDINGS: Proteinuria greater than 3.5g/day Increased WBC COMPLICATIONS: -Accelerated atherosclerosis due to hyperlipidemia -infection due to deficient immune (proteinuria) MEDICAL MANAGEMENT: -The objective is to preserve renal function -diuretics -ACE inhibitor- reduce degree of proteinuria -corticosteroids -antineoplastic agents

Diet: protein 0.85/kg/day with emphasis on high biologic protein such as dairy products, egg & meats Low in saturated fats 3. ACUTE RENAL FAILURE (ARF) -sudden and almost complete loss of renal function over a period of hours to days -manifested by oliguria (less than 400ml/day) Anuria (less than 50ml/day) Rising BUN & creatinine Retention of other metabolic waste (azotemia) 3 MAJOR CATEGORIES OR CONDITION CAUSING ARF 1. Pre-renal occurs as a result of impaired blood flow that leads to hypoperfussion of the kidney and a drop of GFR. Ex. Gastrintestinal losses, vasodilation (shock, sepsis) 2. Intra-renal occur in actual parenchyma damage to the glomeruluss or kidney. Ex. Burns, crash injuries, infection, nephrotoxic agents acute tubular necrosis----loss of kidney function 3. Post-renal- occurs from obstruction somewhere distal to the kidney. 4 PHASES OF ACUTE RENAL FAILURE 1. Initiation: begins with initial insults and ends with oliguria 2. Oliguria- period is accompanied by increase serum concentration usually excreted by the kidney (Urea, BUN, creatinine, uric acid, k, magnesium , organic acid(< 400 ml) 3. diuresis- pt. gradually increasesurine output (sign of GFR recovery) 4. recovery- takes 3-4 months (which result returns to normal) CLINICAL MANIFESTATIONS Lethargy, appears very ill, nausea, vomiting, diarrhea, dry mucous membrane Uremic factor , CNS s/sx Management Identify cause and damage--- treat accordingly PHARMA: hyperkalemiatreated by cation exchange resin ( kayexalate)- work by exchanging Na to K in the GIT (sorbitol)- induce diarrhea type or water Loss effect -- RETENTION ENEMA by rectal catheter (kayexalate) 4. CHRONIC RENAL FAILURE (ESRD)- Progressive, irreversible deterioration in renal function in which the kidneys ability to maintain fluid and electrolyte falls results to uremia or acoismia (retention of urea and nitrogen waste product in the blood) Cause: DM, GN, Hypertensive vascular disease, Polycystic kidney Clinical Manifestations: CVD signs and symptoms, Dermatologic signs, GIT s/sx, CNS s/sx Assessment: GFR. Electrolyte analysis, Anemia Management; Pharmacologic SURGERY: kidney transplant Nrsg. MNGT: pre op/ intra-op, and during post- operative period IMMUNOSUPRESSIVE TREATMENT the survival of transplanted kidney depends on the ability to BLOCK THE BODYS immune response for the transplanted kidney and to overcome or minimize bodys defense mechanism, immunosuppresive agents such as, immuran, azathiopine, cyclosporan are administered 5. INFECTIONS OF THE URINARY TRACT ( Acute and Chronic ) Caused by pathologic microorganism (the normal urinary tract is sterile above the urethra) Lower UTI (structure below the bladder) ystitis (inflammation of the bladder) C Prostitis (inflammation of the prostate gland) Urethritis (inflammation of the urethra) Upper UTI (ureters and kidney) Pyelonephritis (inflammation of renal pelvis)

Interstitial nephritis (inflammation of kidney) Renal abcess Mechanism that maintain sterility of the bladder Physical barrier of the urethra Urine flow (downward) Uretero vesical junction (prevents urine reflux) Various antibacterial enzymes and antibodies Anti-adherent effect mediated by mucosal cell of the bladder PATHOPHYSIOLOGY OF LOWER URINARY TRACT INFECTION Bacterial invasion - Body Defense : shedding of bladder epithelial (remove bacteria) - GAG (Glycosaminoglycan) hydrophilic protein exerts protective effect against bacteria. - NORMAL BACTERIAL flora of vagina & urethra interferes with adherence of e-coli -IgA in urethra provides a barrier to bacteria REFLUX -due to obstruction to urine flow urethra to bladder (urethrovesical reflux) - Body defense: -Cough, sneeze, straining -Increase bladder pressure force urine from bladder to urethra BACTERURIA: Define: Bacteria normally present- urethral area CAUSATIVE AGENTS E. coli - 54.7% Pseudomonas Enterococcus ROUTES OF INFECTION 1. Ascending (up the urethra)= transurethral (fecal contamination) -sexual intercourse/ massaging of urethra forces the bacteria up in bladder 2. Hematogenous 3. Direct extension( (+) fistula from intestine) CLINICAL MANIFESTATION LOWER UTI: over 50% with bacteruria have no symptoms - others: frequent pain & burning sensation on urination; urgency, increase in frequency, nocturia, incontinence & suprapubic or pelvic pain, hematuria, backpain UPPER UTI: fever, chills, flank and low back pain Nausea and vomiting, painful urination (+) tenderness @ cortovertebral angle (+)kidney punch ASSESMENT AND DIAGNOSTIC FINDING TEST: COLONY COUNT: 10 to the 5th power CFU/ml urine - clean catch midstream - catheterization - suprapubic needle aspiration CELLULAR STUDIES: Microscopic hematuria: greater than 4 RBC/ hpf PYURIA: greater than 4 WBC/ hpf URINE CULTURE Recommended for all men and Diabetic with 3 episodes of UTI for the past year, Post-menopausal, Pregnant, women who are sexually active, have new partners And who undergo instrumentation ( catheterization) TESTING METHODS MULTISTRIP DIPSTICK testing for WBC - leukocytes esterase test: ( (+) Patient has pyuria ) - nitrate testing (Griess nitrite reduction test)

(+) if nitrate is reduce to nitrite Intravenous Pyelography(IVP) for high risk and recurrent history of UTI CT scan and Ultrasound MEDICAL MANAGEMENT -Pharma & Px education (infection prevention) -trimethoprim (Trimpex), trimethoprim/sulfamethoxazole (Bactrim, Septra, Cotrim), amoxicillin (Amoxil, Trimox, Wymox), nitrofurantoin (Macrodantin, Furadantin), and ampicillin (Omnipen, Polycillin, Principen, Totacillin) -CRANBERRY extract /juice NURSING INTERVENTION: Relieving pain Management/ monitoring & managing potential complication (RF/ Sepsis) Teaching patient self care = hygiene, fluid intake, voiding habit, complication Recognition and management 6. UPPER URINARY TRACT INFECTION PYELONEPHRITIS Bacterial invasion of the renal pelvis, tubules & interstitial tissue of one or both Kidneys. - Route of Infection: Ascending ( from urethra to the kidneys) - causes: ureterovesical reflux Urinary tract obstruction Bladder tumors Strictures (infant) BPH Stones Acute Pyelonephritis - kidney becomes enlarge with interstitial infiltration of inflammatory cell and abscess are noted. Chronic Pyelonephritis - Scarred, contracted, non- functioning CLINICAL MANIFISTATION ACUTE: Patient appear ill and with chill, fever, pyuria, bacteruria, flank pain & CVA tenderness, Dysuria, frequency in voiding ASSESMENT AND DIAGNOSTIC FINDINGS Ultrasound/ CT/ IVP Urine culture MEDICAL MANAGEMENT Antibiotic (TMP- SMZ, CIFROFLOXACIN,LEVOFLOXACIN for 10 to 14 days CHRONIC : Usually none unless in acute exacerbation - Fatigue/ poor appetite/ polyuria/ thirst/ weight loss Persistence & recurrent infection---- progressive scarring of kidneys--- Renal Failure ASSESSMEN T AND DIGNOSTIC FINDINGS Intravenous Pyelography Blood Urea Nitrogen and Creatinine COMPLICATIONS -End Stage Renal Disease - Hypertension, formation of Kidney stones MANAGEMENT Antimicrobial drugs, teaching patient on bladder emptying, Perineal hygiene 7. Burn Characteristics of Burn According to Depth Burn and causes Superficial Skin involvement Epidermis; Symptoms Tingling Wound appearance Reddened; Recuperative course Complete

Partial Thickness (1st degree burn)

possibly a portion of dermis; most common-sunburn Epidermis; upper dermis portion of deeper dermis

Hyperesthia Pain that is soothed by cooling Pain Hyperesthia Sensitive to cold air

Deep Partial Thickness (2nd degree burn)

blanches w/pressure dry Minimal or no edema Possible blisters Blistered; mottled red base; broken epidermis; weeping surface Edema

recovery within a week, no scarring Peeling Recovery in 2 to 4 weeks Some scarring and depigmentation contractures Infection my convert it to full thickness Eschar sloughs Grafting Scarring and loss of contour and fxn; contractures Loss of digits or extremity possible

Full Thickness (3rd degree burn)

Epidermis; entire dermis, and sometimes subcutaneous tissue; may involve connective tissue, muscle, and bone

Pain free Shock Hematuria (blood in the urine)and possibly hemolysis (blood cell destruction) Possibly entrance and exit wounds (electrical burn)

Dry; pale white leathery, or charred Broken skin with fat exposed Edema

Local and Systemic Response to Burns Burns that do not exceed 25% TBSA produce a primarily local response Burns that exceed 25% TBSA may produce both a local and systemic response and are considered major burn injuries

Cardiovascular Response Hypovolemia is the immediate consequence of fluid loss resulting in decreased perfusion and oxygen delivery Cardiac output decrease before any significant change in blood volume is evident The greatest volume of fluid leak occurs in the first 24-36 hours after the burn, peaking by 6-8 hours

Burn Edema Edema maximal after 24 hours It begins to resolve 1-2 days post burns and usually is completely resolved in 7-10 days post injury Edema increase in circumferential burns, pressure on small blood vessels and nerve in distal extremities cause an obstruction of blood flow and consequent ischemia

Effects on Fluids and Electrolytes and Blood Volume Evaporative fluid loss through the burn wound may reach 3 to 5 L or more over a 24 hour period until the burn surfaces are covered

Hyponatremia is most common during the first week of the acute phase, as water shifts from the interstitial to the vascular space Immediately after burn injury, hyperkalemia (excessive potassium) results from massive cell destruction. Hypokelamia (potassium depletion) may occur later with fluid shifts from the interstitial to the vascular space

Pulmonary Response Inhalation, bronchoconstriction caused by release of histamine, serotonin and thromboxane a powerfull vasoconstrictor, as well as chest constriction secondary to circumferential full thickness chest burns caused this deterioration Pulmonary, upper airway injury results from direct heat or edema, manifested by mechanical obstruction of the upper airway Carbon monoxide, the pathophysiologic effects due to tissue hypoxia, a result of carbon monoxide combining with hemoglobin to form carboxyhemoglobin, which competes with oxygen for available hemoglobin binding sites Other Systemic Response Renal fxn may be altered as a result of decreased blood volume, destruction of red blood cells at the injury site results in free hemoglobin in the urine Significant impairment of the production and release of granulocytes and macrophages from bone marrow after burn injury. The resulting immunosup pression places the burn patient at high risk of sepsis Loss of skin also results in an inability to regulate body temperature. Burn patients may therefore exhibit low body temp. in the early hours after injury Two potential gastrointestinal complications may occur, paralytic ileus and Curling ulcer, gastric distention and nausea my lead to vomiting unless gastric decompression is initiated

Phases of Burn Care Phase Emergent or immediate or resuscitative Duration From onset of injury to completion of fluid resuscitation Priorities First aid Prevention of shock Prevention of respiratory distress Detection and tx of concominant injuries Wound assessment and initial care Wound care and closure Prevention or tx of complication, including of infection Nutritional support Prevention of scars and contractures Physical, occupational, and cosmetic reconstruction Psychosocial counselling

Acute

From beginning of diuresis to near completion of wound care

Rehabilitation

From major wound closure to return to individual optimal level of physical and psychosocial adjustment

Emergency Procedure at the Burn scene Extinguish the flames Cool the burn Remove restricted objects Cover the wound Irrigate chemical burns

Emergency Medical Management Transport to the nearest emergency department Prioritize the airway, breathing, and circulation Administer humidification, bronchodilator, mucolytic agents Continuous + airway pressure and mechanical ventilation may also be required to achieve adequate oxygenation Asses for cervical spinal injuries Asses for burn and wound Insert IVP and NGT, and suction the pt. to prevent vomiting Practice aseptic technique to prevent infection Asses for TBSA Fluid replacement Asses for Acute Respiratory and Renal Failure Transfer to a burn center Management of fluid loss and shock

Acute or Intermediate Phase of Burn Care Infection prevention Phase occur 48-72 hours after burn injury Asses for electrolytes imbalance, and gastrointestinal fxn Infection prevention,wound cleaning, topical antibacterial therapy, wound dressing, wound debridement, and wound grafting Pain management and nutritional support Asses for airway obstruction caused by upper airway edema Asses for capillaries integrity Monitor fever for the signs of infection Monitor for infection like staphylococcus, proteus, pseudomonas, Escherichia coli, klebsiella, candida albicans, Wound Cleaning Hydrotherapy Use tap water Tub baths Topical Antibacterial Therapy Silver sulfadiazine (silvadene) Mafenide acetate (sulfamylon) Silver nitrate Acticoat

Wound Dressing

1st topical agent is applied then covered by a several layers of dressing A light dressing is also applied areas for which a splint has been designed to conform to the body contour -the proper positioning

Dressing Change Dressings are changed in the pt. units, hydrotherapy room, or tx approximately 20 min after an analgesics agent administered They may also changed in the OR after the pt. administered anesthesia

Wound Debridement To remove tissue contaminated by bacteria and foreign bodies, thereby protecting the pt. from invasion of bacteria To remove devitalized tissue or burn eschar in preparation for grafting and wound healing Natural debridement Mechanical debridement Surgical debridement Management 1. First aid Put out flames by rolling the child on a blanket Immerse the burned part on a cold water Remove burned clothing Cover burns with sterile dressing 2. Maintenance of a patent airway Suction secretions prn O2 administration with humidity Tracheostomy or ET intubation 3. Prevention of Shock, Fluid and Electrolyte Imbalance Isotonic saline or LR to replace electrolytes Colloids to expand blood volume Dextrose in water to provide calories FLUID RESUSCITATION: PARKLAND FORMULA Plain LR 4ml X body wt (kg) X TBSA burned of total: 1st 8hrs post burn of total: 2nd & 3rd 8hrs post burn Goal: U.O.= 1ml/kg/hr 4. Booster dose of tetanus toxoid 5. Relief of pain such as IV analgesic (Morphine SO4) 6. Prevention of wound infection Wound cleaning and debriding Open and close method of wound care Whirlpool treatment 7. Skin grafting: From buttocks or xenograft, frozen cadaver 8. Diet: calorie, protein Burn Prevention Tips Keep matches and lighters out of reach of the children Never leave unattended around fire or in bathroom/bathtub

Install and maintain smoke detectors in the home Develop and practice and practice home exit fire drill Set the water heater temperature no higher than 120F Do not smoke in bed. Do not fall asleep while smoking Do not throw flammable liquids on to an already burning fire Do not use flammable liquids to start fires Do not remove radiator cap from a hot engine Watch for overhead electrical wires and underground wires when working outside Never store flammable liquids near a fire source, such as a pilot light Use caution while cooking Keep a working fire extinguisher in your home

Area Head (A/D) Thigh (B/E) Leg (C/F)

By age in years 0 1 5 10% 9% 7% 3% 3% 4% 2% 3% 3%

10 6% 5% 3%

8. DIARRHEA in stool frequency (>3-5x/day) with water content 2 Types Acute diarrhea CNSD (Chronic Non-Specific Diarrhea) Associated with Gastroenteritis: bacteria, virus, fungi Dietary causes: overfeeding, excess sugar in formula, intro of new foods Meds: laxatives and antibiotics

 Amox, Ampi, Pen Poisoning: Arsenic, Lead, Mercury, Organophosphate CNSD Or Irritable Colon of Childhood or Toddlers Diarrhea Associated with Food (Lactose) intolerance Excessive softdrinks/ fruit juices: sorbitol and fructose fat diet: restricted dairy and milk products *osmotically active, CHO, e+ Associated with contaminated water 2 wks duration, no S/Sx of malnutirition, enteric infection and dehydration rate of gastric emptying and intestinal transit time ASSESSMENT u.o., weight, (-) tears, (-) saliva, dry mucous membranes, poor skin turgor, sunken fontanel, pale cool dry skin Severe DHN: BP, HR, RR, >2sec CRT (impending shock) COMPLICATIONS 1. Dehydration Mild: 5-6%, thirst, slighty dry buccal mucosa Moderate: 7-9%, (-) skin turgor, sunken eyes and fontanel Severe:>9%, S/ of moderate DHN + one of the following Rapid, thready pulse RR Lethargy to coma Severe metabolic acidosis 2. Electrolyte Imbalance Metabolic acidosis (H+) Respiratory alkalosis 3. Malnutrition Due to dietary intake, malabsorption syndrome and catabolic response to infection MANAGEMENT Oral Rehydration Solution (ORS): Pedialyte, Hydrite, Infalyte, WHO), rice-based ORS as substitute Tx of choice for mild to mod DHN Physiologic basis: glucose-mediated solution Na+ absorption Most effective, less painful, less costly than IV Replace stool losses with .-1 cup ORS IV (plain LR or D5NSS) For severe DHN with shock: 20-30 cc/kg bolus Anti-diarrheal meds (Lomotil, Imodium) not recommended: worsen diarrheatoxicity and ADR due to motility, ileus may occur NURSING CARE Assess hydration status, weigh OD, I/O, urine specific gravity Continue breastfeeding and usual diet Skin care on perianal area (Zinc oxide cream) No rectal T!: stimulate bowel and stool passage Hand washing, proper disposal of diapers