CRITICAL CARE NURSING Encoded by/Property of: Ryan Mendoza Ecunar, SLU SN IV The critical care environment Fast-paced

Highly specialized Technical o Technolo gically advanced o Skilled nurses Requires various types of equipments Necessary supplies must be easily and quickly accessible o Nurse patient ratio is 1:1 or 1:2 o In RP, 1:4 Pts. Are cared for individually and uniquely In life and death situations c supportive devices c multiple complications in intensive ttt for sp ecific dysfxs Assessment 1. Nursing history May have direct admission CC nurse i ntegrates data for pt and family, written hx and the transfer report o E.g. HPNHPI Diet Smoking ROH use Stress 2. Diagnostics ECGs Respirations Intraarterial P Pulmonary artery P Venous O2 sat Body temp Continuous Airway P M o Non-invasiv e technique that uses a transducer cable, d P tubing & a display monitor o The w aveforms produced by the system enable the clinician to continuously M the pts. Response to various modes of mechanical ventilation o d P- kinks and destruction s Sources of obstructions: phlegm NR: y Look for kinks y Suction the pt o d P- c ause by detached tubing, leak from the mechanical ventilator CVP M o Maybe used in lieu of a pulmonary artery catheter when evaluation of pulmonary artery P and L sided heart failure are nor reqd o Unit in cmH20 o 0-25 calibrations o Normal: 4-l2 cmH20 other books, 4-10 0r 6-12 cmH20 o If below: hypervolemia o If above: hypovolemia Intracranial P M o Involves placing a catheter through the skull in to either the subarachnoid space or the cerebral ventricle to M changes in P wit hin the cranial cavity o A transducer and tubing system gather the data cc are d isplayed on the M screens o In RP, Cushings triad o If widening pulse P, Increase d ICP o If narrowed pulse P, shock compensation

o Pulse Pressure= BP Systole - Diastole Cardiac Monitoring o A non-invasive proc edure that poses minimal risk to pt o Placing conductive electrodes on the pts c hest that recognizes the electrical activity of the heart and relay it to a vide o display screen o Review placement of electrodes o NOTE: if status post op, c b reast CA, okay electrodes at the back Hemodynamic M o Invasive M of the arterial or venous system o M is accompanied through catheters that measure changes in a ir and fluid P o Can also be used to administer IVFs and certain arterial and/or venous blood for lab analysis o 2 types commonly used: Intraarterial M y Cathet er is inserted into an artery radial or femoral connected to a high P flush syst em filled c either non/heparinized saline solution y Intraarterial systems displ ay a continuous reading of the pts BP y Transducers are connected to the system that interprets the air and fluid P readings and display results as waveforms on cardiac monitoring equipment Pulmonary artery M y Involves inserting a catheter via the subclavian or internal jugular vein and advancing it into the pulmonary artery Teaching in the CCU is focused on the short term. The nurse communicates to the pt and the family 1. 2. 3. 4. 5. rationale for the ttts, procedures and medicati ons plans for ongoing care goals for ttt interpretations of the dx, dx tests and expectations resources available foe financial, coping, support and other perso nal needs Abdominal aortic aneurysm (AAA assoc c atherosclerosis (most common cause) and H PN common to adults 70 y/o and above ng age and smoking contributes as well 90 % develop below the renal arteries, usually where the abdominal aorta branches fr om the iliac arteries Risk factors HTN (more than have HTN)

Genetic predisposition Caucasian race Cystic medial necrosis Athero/arterisclero sis Immunologic conditions Male four times than women Advancing age Pregnancy Co ngenital defects of the aortic valve Coarctation of the aorta Inflammatory aorti tis Syphilis Trauma Local infection (pyrogenic or fungal) mycotic aneurysm ALERT: No deep palpation!!! Diagnostics 1. CT scan/ MRI 2. Angiography- uses contrast dye solution injected into the aorta or involved vessel to visualize the precise size and location of the Aneurysm 3. abdl UTZ- to dx AAA 4. transesophageal achocardiogram- to differ entiate 5. CXR Nursing Responsibilities 1. in aortic dissection a. IV beta block ers (Esmolol) b. Na nitroprusside (similar c Dep patch) c. CCBs d. Avoid giving direct vasodilators further destruction injury e. Post-operative anticoagulants i. Heparin ii. Low dose ASA tx 2. Surgery a. Post-op care b. M u/o c. M FE imbal ance d. M graft leaks i. Ecchymosis of the scrotum and perineum (penile area) ii . ng abdominal girth iii. Weak and absent peripheral pulses iv. Fall in Hgb and Hct v. Pain over the pelvis, back and groin vi. Decreasing u/o vii. Decreasing h emodynamic M Nursing Diagnoses risk for ineffective tissue perfusion risk for in jury anxiety Acute Respiratory Distress Syndrome Pathophysiology Pulmonary insul t Chemical mediators released Damage to alveolar capillary membrane Interstitial edema alveolar edema damaged surfactantproducing cells d surfactant production Aneurysm- abN dilation of the BVs - commonly affects aorta and peripheral arteri es - may also develop in the ventricles - forms due to weakness of the arterial wall - HTN is a major contributing factor - destruction of the collagen and elas tin Collagen- s tensile strength of the vessel- preventing dilation Elastin- all ows recoil 1. primary component of the intimal wall and medial layers Types: 1. True Aneurysm a. brought abt by the eroding effects of atherosclerosis and HTN b . affects the 3 layers of the vessel wall and most are Fusiform or circumferenti al i. Fusiform- spindle shape and taper at both ends ii. Circumferential- involv es the entire diameter of the vessel 2. False Aneurysm a. also known as the trau matic Aneurysm bec of traumatic break in the vessel wall rather than weakening b . usually are saccular- like small outpouchings i. Berey Aneurysm- type of saccu lar Aneurysm but relatively small (2 cm in diameter) ii. Dissecting Aneurysm 1. develops when a break or tear in the tunica intima and media allows blood to inv ade or dissect the layers of the vessel wall 2. blood accumulates in the adventi tia and thus form a saccular or a longitudinal aneurysm Aortic Dissection - a li fe- threatening condition a tear in the artery inner layer allows blood to disse ct or split in the vessel wall manifestation is epigastric pain Clinical manifes tations Asymptomatic Pulsating abdominal mass in the middle and upper abd when l ying down, bruit is heard Intermittent and constant pain over the midabdominal a rea region and lower neck (if pain is present) Pain may range from mild discomfo rt to severe (depending on the size) severe pain may indicate impending rupture Dilution of surfactants d lung compliance, atelectasis, hyaline membrane formation d work of breathing i mpaired gas exchange RESPIRATORY FAILURE Acute Respiratory Failure consequence of severe respiratory dysfx defined by arterial blood gas values o an arterial 02 level of <50-60mmHg o an arterial CO2 level of >50mmHg in COPD o acute drop in blood O2 levels

o increased CO2 levels failure of O2- hypoxemia s a rise in CO2 levels hypoventi lation- hypoxemia and hypercapnia acute lung injury Mortality due to multiple or gan system dysfx AKA adult hyaline membrane dse charac by noncardiac pulmonary e dema and refractory hypoxemia

usually superficial involving the epidermis e.g. solar, x-rays, radioactive agen ts Manifestations dyspnea tachypnea anxiety restlessness apprehension impaired judg ment motor impairment tachycardia HTN Cyanosis Dysrhythmias Hypotension Decrease d cardiac output Tissue hypoxia Metab acidosis Develop within 24-48hourss p init ial insult Progressive respiratory distress Cyanosis does not improve c O2 admin Medications Nitric oxide reducers (nitrous oxide a free radical) Surfactants In flammatory blockage utilizing steroids Mech vent Nutrition eat PO, enteral and p arenteral feeding Review arachidonic acid pathway!!! Burns An injury resulting fr exposure to heat, chemicals, radiation or electric curren t A transfer of energy fr a source of heat to the human body initiates a sequenc e of physiologic event in the most severe cases leads to irreversible tissue des truction Types of Causative agents of Burns 1. thermal most common injury dryheat: open f lame moist heat: steam, hotliquids 2. chemical caused by direct skin contact c a cids, strong alkali, organic compounds chemicals destroy tissue CHON leading to necrosis e.g. inhalatory (cement) burns 3. electrical depends on the type and du ration of current and amount of voltage difficult to assess because the destruct ive processes are concealed entry and exit wounds tend to be small, masking a wi despread tissue damage underneath the wound eg. Direct and alternating current, lightening 4. radiation usually assic c unburn and radiation fr ttt of cancer Factors Affecting Burns Depth of the burn (layers of underlying tissue affected) o Det by the elements of the kin that have been damaged or destroyed Characs of Burns by Depth Superficial (epidermis): skin maybe pink to red and dry usually heals in 3-6 days peeling of the skin is evident e.g. sunburn redness, mild edem a, pain and increased sensitivity to heat desquamation is 2-3 days Partial thick ness (epidermis and dermis):maybe superficial and deep partial thickness Superfi cial: involves the dermis and the papillae of the dermis Burn is often bright re d but has a moist glistening appearance c blister formation Burnt area will blan ch when P is applied; touch and pain sensation remain intact Heals in 21days c m inimal or no scarring Upper 3rd of the dermis Good blood supply Blisters Nerve e ndings are exposed painful Deep partial thickness: involves entire dermis but ex tends further Sebaceous glands and epidermal sweat glands remain intact Surface of the skin appears pink and waxy and may be moist or dry Capillary refill is de creased and secretions to deep P is present Requires more than 21 days to heal ( 3-6 weeks) c scar Can proceed to full thickness due to infection, hypoxia or isc hemia Contactures, hypertrophic scarring Full thickness: epidermis, dermis, unde rlying tissues: skin appears waxy, dry, leathery, charred Involves all layers of the skin, including the epidermis, dermis and the epidermal appendages It can e xtend to the SQ, connective tissues, muscle and bone Hard, dry, leathery eschar Eschar- dead tissue, must be removed Grafting to heal Deep full thickness wounds Extend beyond the skin to underlying tissues and fascia, muscles, bones and ten dons Complete absence of sensation Extent of the burn (percentage of body surfac e area involved) o Expressed as a % of the total body surface area (TBSA) use ru le of nines (prehosp) Extent of Burns- expressed in % of the TBSA Rule of Nines- emergency outside the

hospital; rapid

Lund and Browder method- det surface area measurement for each body part accdg t o cts. Age Parklands Formula = 4 mL x TBSA x wt kgs. ABLS formula = 2- 4mL x TBSA x wt kgs.pt Curlings Ulcer- brought abt by stress Classification of Burn Injuries by Extent Minor burn injuries i. excludes electr ical and inhalational and complicated injuries such as trauma ii. partial thickn ess burn of less than 1% of TBSA iii. full thickness burn of less than 2% of TBS A iv. e.g 1. sunburn- exposure to UV light; most common 2. scalding burns Zone o f hyperemia Zone of Stasis- with inflammatory by-products Moderate burn injuries i. excludes electrical and inhalational and complicated injuries such as trauma ii. partial thicknessof 15-25% iii. full thickness burns of less than 10% TBSA Major burn injuries i. includes all burnsa of the hands, face, eyes, ears, feet and perineum, all electrical injuries, multiple traumas, and all cts. That are c onsidered high risk Burn Stages 1. Emergent/Resuscitative stage a. Fr onset of the injury through su ccessful fluid resuscitation b. HCWs estimate the extent of burn injury c. Insti tute 1st aid measures d. Ct may be intubated 2. Acute stage- start of the diures is and ends c the closure of the wound, either by natural healing or by using sk in grafts 3. Rehabilitative stage a. Begins c wound closure and ends when the ct returns to highest level of H restoration, cc may take years b. CT and PT may b e needed i. ROM exercises ii. Splints to prevent contracture deformities and com partment syndrome Pathophysiologic Effects of a Major Burn (Refer to Lippincott Manual of Nsg Practice 8th ed, start pp1122)

Burn Wound Healing 1. Inflammatory a. Immediately ff the injury, plts. Coming in contact c the damage tissue aggregate b. Fibrin is deposited, trapping further plts. And thrombus is formed (clamping) c. Hemostasis is maintained by the throm bus and vasoconstriction d. Vasodilation occurs and increases vascular permeabil ity e. Neutrophils infiltrate (24 hours) then is replaced by the monocytes and c onverted to macrophages that consumes the pathogens and dead tissue f. Also stim ulates the proliferation of fibroblasts g. Angiogenesis promoted by VEGF apoptos is 2. Proliferation a. Within 2-3 days p burn b. Granulation tissue begins c com plete reepithelialization c. Epithelial cells cover the wound 3. Remodelling a. Lasts for years b. Collagen fibers laid down c. Scars contact and fade in color d. Hypertrophies scar and keloid may appear e. Hypertrophic scar i. Is an overgr owth of dermal tissue that remains within the boundaries of the wound f. Keloida scar that extends beyond the boundaries of the original wound Skin Changes o Epidermis- outer layer o Dermis- 2nd layer Made up of collagen, f ibers, CTs and elstic fibers Within it are BVs, sensory nerves, hair follicles, sebaceous and sweat glands Functional Changes o Evaporation o Skin can tolerate up to 40degs o 71deg C and above will cause cell destruction cc is so rapid Vasc ular Changes o Fluid shifts 3rd spacing due to extravasation Edema Hypovolemia H yperkalemia Hyponatremia hemoconcentration Fluid remobilization o Diuretic stage - 48 to 72 hours o Hyponatremia o Hypokalemia o Hemodilution o Metabolic acidosi s o GIVE: colloids (Zenalb- in 5% or 25 % prep) albumin maintains Oncotic pressu re pulling P Cardiac changes Cardiac Output (CO) d circulation vasomotor rxn (va socons) Baroreceptors stimulated stimulus Medulla oblongata impulse Release of c atecholamines PNS (Epinephrine and Norepi) Effect of sympathetic response Increa sed Heart rate stimulus Adrenalmedulla Pulmonary changes o Cause of death (CO po isoning) more than 60 % CO DEATH o Upper airway affected by inhaled smoke that c auses edema then obstruction 10% is confusion, delirium, etc, 40% comatose Injur y

Increased histamine production Increased VP EV Alveolus Congestion CO and CO2 ex change impairment GI Changes o Decreased perfusion to the GI tract o Sympathetic response o Curlings Ulcer- due to BV (compensation) increased Cardiac output epi nephrine release Increased GI mobility Increased HCl release invitation Shock y Eg. Jobst support garment Used for 6 mos to a year

state which develops where there is inadequate tissue perfusion causing the cell s to be deprived of adeq 02, convert to anaerobic metabolism resulting in the pr oduction of lactate and acidosis 500 cc is adeq volume to manifest shock Compensatory Mechanisms Inflammatory compensation Sympathetic nervous system sti mulation Nursing Diagnoses Decreased cardiac output r/t altered stroke volume fr an increased capillary permeability Body image disturbance Pain Impaired tissue perfusion FVD/FEI ATR- initially, hyperthermialate, hypothermia Impaired skin in tegrity High risk: infection (high risk- preventable, foreseeable crisis, no s/s x yet Interventions fluid tx plasma exchange tx M o/u Management pain control te tanus prophylaxis nutritional support prevent gastric acidity to prevent Curlings Ulcer o PPIs, H2 receptor inhibitor, antacids, Antimicrobials o silver sulfadiaz ine o silver nitrate Surgery o Escharectomy o Debridement Removal of wound debri s and eschar Has 3 types Mechanical y y Enzymatic y Surgical o Skin Grafting Aut ograft Homograft/allograft (cadavers) Heterograft/ xenograft (animal)- pigs Woun d Mx o Dressing the wound Open- apply antimicrobial and expose Close- allocate P dressings to prevent scar and keloids o Positioning, splints, exercise and cont ractures o Support garments Applied 5-7d p grafting Maintaining 10-20 mmHg to co ntrol scarring Classification of Shock 1. Hypovolemic shock- extremely lowered ciculating blood volume (due to hemorrhage, internal andextravascular loss) 2. Cardiogenic shock a. inability of the myocardium to pump an adeq cardiac output to maintain tissu e perfusion b. happens when myocardial fx is depressed, several compensatory mec hanism are activated c. sympathetic stimulation increases heart rate and contrac tility, and renal fluid retention increases preload (tachycardia and effects of RAA mechanism) and cause selewctive vasoconstriction d. Renin-angiotensin-Angiot ensinogen System Cardiac output kidneys ( perfusion) juxtamedullary nephrons Ren in secreted fr the kidneys Aldosterone Na and water retention Increased BV Incre ased BP Angiotensin 1 ACE in lungs Angiotensin II VC Increased BP Causes/Etiology of Cardiogenic shock most common cause is the loss of 40-50% of viable myocardial tissue Mechanical Px o Valvular heart dses o Perforated intrav entricular septum o Papillary muscle dysfx/rupture o Myocardial rupture o Syphil is a spirochete destroys myofilaments Shock and aneurysm o Cardiomyopathies o Hy povolemia o Metabolic dysfx o Vasomotor dysfx o Microcirculatory dysfx 3. Extrac ardiac obstructive shock- physical condition to flow (ie. Tension Pneumothorax, dissecting AA and pulmonary embolus) 4. Distributive shock a. abN distribution o f intravascular vol. b. includes the ff i. Septic shock 1. more on G- bacteria a . blows off O2 increased RR resp alkalosis 2. endogenous pyrogenes EARLY/ WARM s tage Hypothalamus

progresses LATE/ COLD stage Increased temp friction ability Dilation, etc 3rd spacing Decreased cardiac output Metabolic acidosis 3. Coagula ting fx XI- Hageman factor Complement sys kinin sys fibrinolytic cascade clottin g Interferons serotonin Protrombin and thrombin (natural antiviral) bradykinin h istamine ii. Anaphylactic shock iii. Neurogenic shock Manifestations 1. Compensa tory Phase a. tachycardia (compensation 2 sympathetic stimulation and RAA system b. bounding pulse c. tachypnea (compensation for hypoxia and excessive amounts of CO2) d. restlessness and irritability (resulting fr cerebral hypoxia) e. decr eased U/O, cool and pale skin (vasoconstriction) f. epinephrine SNS tachycardia BP 2. Progressive stage a. HPoN (failing compensatory mech) i. MAP <60mmHg but m anifestation of HPoN reveals if arterial P is <40mmHg b. Narrowed pulse P c. Dec stroke vol- weak, rapid and thready pulse saused by decreased cardiac output d. Shallow resp e. Weakness progresses f. Dec renal output g. Respiratory acidosis 3. Irreversible stage a. Unconsciousness reflexes (A_B/ Electrolyte imbalance) b. HPoN worsens (decreased cardiac output) c. Slow, Cheyne-stokes respiration (2 to resp center depression) d. Anuria (renal failure) i. Diff: oliguria- 100-400 cc/24 hours vs. ii. Anuria- 5-10 cc/24hours Diagnostic Examinations CBC- hct (c oncentration of compositions, plasma) levels may be d due to hemorrhage o d Hct nay mean DHN o d overload ESR- if elevated- due to injury and inflammation, indi cates infection BUN and Creatinine clearance- elevated due to d renal perfusion Lactate- elevated sec to anaerobic metabolism Glucose levels- elevated due to re lease of glycogen sec to sympathetic response ABGs o Resp alka in early stages a ssoc c tachypnea Resp acidosis in later stages due to respiratory depression o Metabolic acidosis in later stages sec to anaerobic metabolism Urinalysis- increased specific grav ity due to effects of ADH CXR- pulmonary congestion latter stages ECG- dets MI ( elevation of ST segment, widening of QRS complex, overriding U) heart rate and i schemic changes o Pathophysiologies of Shock 1 Marked d cardiac output Cardiac index (% cardiac ou tput dist to systemic circu) < 1.8 L/m/m2 d coronary blood flow Compensatory mec hanism occur (increase VR and catecholamine) Increased pload inc contractility ISCHEMIA 2 L vent and diastolic P Pulmonary P s Pulmonary edema cavity distentio n dec pload endocardial ischemia Increased arterial hypoxemia pulmonary artery P cellular acidosis Ischemia and R Vent failure fluid retention may increase volume to the pt where pulmonary cong estion and hypoxemia occur iscgemia also s ventricular diastolic compliance, fur ther elevating L atrial P worsening pulmonary congestion Effects of Vasoconstriction vasoconstriction cc is the effect of systemic vascul ar resistances, increases myocardial pload, further impairing cardiac performanc e and increasing myocardial o2 demand further causing worsening ischemia and fur ther to pts. demise vasoconstriction to maintain BP can compromise multisystemat ically (renal, splanchnic and cutaneous perfusion) Medical Mx id underlying caus e if possible o Streptokinase and Urokinase Thrombolytics Intubation, mech vent and suppl O2 to increase oxygenation Improve O2 content (Hgb and arterialO2 sat) Continuous cardiac M- detects changes in heart rate and rhythm Two (2) IV lines c large gauge needles (g 14-16, in RP only 18 is available) for fluid and drug admin IV fluids (crystalloids) to maintain and Increase intravascular volume Med ications Inotropics- increases heart contractility and cardiac output o Dopamine (has Calcium) o Dobutamine and Epinephrine Vasodilators

o o Given c vasopressors to decrease the ventricular workload Only for cardiogenic s hock Nitroglycerine and nitroprusside Has vasodilatory effects towards periphera l circulation Decreased vascular resistance

Decreased stroke volume Thrombolytic Tx o For coronary revascularization to allo w restoration of coronary artery blood flow o Streptokinase/ Urokinase o NOTE: I f MI lasted already for 12 or 6 hours, dont give T tx anymore because the myocard ium is already dead! Diuretics- If c fluid overload to decrease ventricular work load For septic shock: o Give antibiotics o Antipyretics due to fever vasodilato ry effects o BT whole blood and its by-products PRBC WB Plt. Concentrate FFP als o has cryoppts and plt (for DICcryoppts has clotting factors 10-20 cc to be used ) o Osmotic diuretic maybe needed to increase renal bloodflow and U/O Adenohypophysis/ Anterior Pituitary Gland: FAT-LPG-Me o F- Follicle-stimulating hormone o A- Adrenocorticotropic hormone o T- Thyroid-stimulating hormone o L- L uteinizing hormone o P- Prolactin o G- Growth hormones o M- Melanocyte stimulati ng hormone Posterior hypophysis/ Posterior pituitary gland: Anti-Oxy o A- Antidi uretic Hormone o O- Oxytocin

Nursing Management MVS q 15min o <80 mmHg usually results in inadequate coronary artey blood flow (incr in O2 flow if blood P is <80 mmHg then notufy the physic ian immediately) M ECG tracings continuously Hemodynamic M o CVP, RV P, Pulmonar y artery P, Pulmonary wedge P, L atrial P and CO M U/O Maintain patent airway an d adequate ventilation M serum levels M skin color and temp and note changes o C old clammy skin is maybe a sign of continuing peripheral vascular constriction, indicating progressive shock M arterial blood samples o to increase ABG levels o ABG results are the determinant for O2 manipulation Provide psychological suppo rt- reassuring ct. to relieve apprehension and keep family advised Minimize fact ors contributing to shock o Elevate lower extremities to 45 degs to promote veno us return o Avoid trendelenburg position bec it increases respiratory impairment o Just position the pt to modified trendelenburg position : PILLOW o Promote ad equate rest by using energy conservation measures and maintaining a restful and quiet envt. Mneumonic of Hormones and their Origin Diabetic Ketoacidosis Causes infection Illness Surgery Stress Insufficient or ab sent insulin Assessment Findings Kussmauls breathing Fruity breath odor 3 Ps Wt lo ss Muscle wasting Leg cramps Treatment rehydration PNSS IV insulin M blood gluco se Assess LOC and patent airway MVS for DHN restoration of acid-base balance and electrolyte balance control of glucose level (insulin drip) or sliding scale fo r Hyperkalemia: o Kayexalate tx (Enema) excretion of K o Gics solution admin of hyperosmolar solution plus insulin in D50-50 o Aerosol tx (salbutamol)- a sympat omimetic drug Excretes K (no need for resting) Adequate contraction of the heart Bronchodilation Addisons Disease primary adrenocortical insufficiency, hypofx of the adrenal cortex causes decreased production of hormones Assessment fatigue, muscle weakness anorexia, N/V, wt loss hypoglycemic reactions hypotension, weak pulse decreased capcity to deal c stress low cortisol levels bronzelike pigmenta tion of the skin common to 2o Secondary:ACTH and low adrenal gland fx Sugar Sex salt Primary: ACTH px AG fx Sugar Sex salt Nursing responsibilities: Hormone rep lacement o Glucucorticoids Decadron (dexamethasone) hydrocortisone o Mineralocor ticoids (fludrocortisones acetate) MVS and I&O

Decrease stress in the envt Prevent exposure to infxn and heat (hot weather) Rest periods, prevent fatigue Weigh daily Provide small freq feedings (high in CHO, Na and CHON) to prevent hypoglycemia and hyponatremia Addisonian Crisis severe exacerbation of adddisons dse caused by acute adrenal in sufficiency Precipitated by o Strenuous activities o Infxn (pneumonia) o Trauma o Stress and failure to take meds o Iatrogenic: surgery on pituitary gland or ad renal glands, rapid cdrawal of exogenous long time steroid use Assessment severe generalized muscle weakness hypotension hypovolemia shock due to vascular colla pse Nursing responsibilities admin glucucorticoids (hydrocortisone) and IVFs to maintain hydration abt 3-5 liters of saline strict bedrest and eliminate all for ms of stressful activities MVS and I&O, weigh daily Protect fr infxn Assess for fluid balance (increase in fluid intake during the hot weather due to increase i n perspiration) Thyroid Storm uncontrolled life threatening hyperthyroidism caus ed by excessive release of thyroid hormone commonly caused by stress, infection and unprepared thyroid surgery S/Sx o Apprehension o Restlessness o Extremely hi gh temp of abt 40 deg C o Tachycardia o CHF o Resp distress o Delirium o Coma Nu rsing responsibilities maintain a patent airway and adequate ventilation O2 and IV tx Admin anti thyroid drugs, sedatives and cardiac drugs Give INDERAL Control fever c non ASA drugs (it competes c thyroxine site storm) Pancreatitis inflame process c varying degrees of pancreatic edema inflame of the pancreas that may result to autodigestion of the pancreas by its own enzymes leading to hemorrhage and necrosis occurs most often in men in the middle ages Alcoholism is the most common cause Other causes: o Biliary tract dse o Trauma o Drugs Etiology and Risk factors 1. ROH abuse- causes physiochemical alteration of CHON that plugs the pancreatic ductules (sphincter of Oddi) 2. Gallstones- when a st one migrates through the ampulla of Vater 3. abdl trauma 4. hyperlipedemia 5. hy percalcemia 6. familial causes 7. Pancreatic trauma 8. pancreatic ischemia Asses sment LUQ pain mid-epi of the LUQ that radiates to the back and L shoulder and L flank Pain is continuous and is worsened by lying down in supine position FETAL POSITION is the most comfortable position for them Wt loss due to N/V Steatorhh ea Abdominal assessment o Generalized jaundice o Cullens sign grey blue discolora tion of the flank o Low bowel sounds due to paralytic ileus o Abdominal tenderne ss, rigidity and guarding the peritoneum o VS M impending shock Laboratories ser um amylase-2-12 hours fr onset of the mainifestations serum lipase- on of the mo st specific indications bec it is solely the Pancreatitis (7h-2d) WBC- above 10, 000mm3 Hyperglycemia hypocalcemia Types of Pancreatitis 1. Acute Pancreatitis a. apigastric pain radiating to the back b. Cullens Sign (purpura around the umbili cus) c. Turners sign (violet discoloration/ ecchymosis at the L flank) d. Elevat ed pancreatic enzymes (lipase and amylase) e. MX: i. NPO ii. IVF iii. NGT iv. TP N as a last resort most common compli of this is hyperglycemia v. Avoid ROH 2. C hronic Pancreatitis a. Abdl pain or tenderness (LUQ) b. DM c. Mx: i. High calori e diet, low fat ii. Avoid ROH iii. Admin pancreatic enzymes iv. glucoseMx Pathop hysiology Trypsin by HCl Protelytic enzymes and lipolytic enzymes Prematurely ac tivated in the pancreas Tissue damage Interventions

Comfort Measures o Knee chest position or side lying position c pillow pressed a gainst the abd TPN During the recovery phase when food is tolerated give small f req feeding mod to high CHO, high CHON, low fat meals Food shld be bland c liitl e spice Caffeine (tea, etc._ shld be avoided GI irritants ENSURE (directly absor bed amino acids) AVOID ROH Fasting- to rets the pancreas and dec Pancreatic enzy me action IV- for rehydration Meperidine- drug of choice Morphine- contraindicat ed because spasm of the sphincter of Oddi can potentiate parenchymal injury Ca a nd MgSO4 IV replacement Gastric decompression- prevents gastric digestive juices fr flowing into the duodenum NGT drainage and suction- for continuous V/ give D EMEROL Food in the duodenum CCU cells PZ cells Stimulated Gallbladder Release bi le Bile salts pancreas release enzymes Pancreatitis Renal Failure and End-stage Renal Dse early sign is albuminuria (cloudy in appea rance) N, K and CHON are absorbable in kidneys Acute Renal Failure is the rapid decline of renal fx c azotemia (presence of urine by-products in the blood) and fluid and electrolyte imbalance onset is sudden (hours to days) % of nephron inv olvement : 50 % Duration is 2-4 weeks to less than 3 months Prognosis- good if n ephron of renal fx c supportive care, high mortality in some situations Causes R enal infection o take full course antibiotics and drink at least 3L of h2o every day prevents ARF (abt 8-10 glasses) NSAIDS o vs COX1 dec BV dec CO tissue hypoxi a (give Na and H20 tx) DM o High glucose level inc tonicity of the circulation d ec perfusion formation of plaques in the intimal wall of glomerolus dec GRF RF H TN Glomerulonephritis Types of ARF 1. Pre-renal failure- inadequate kidney perfu sion a. due to heart failure, etc 2. Intrarenal or intrinsic renal failure damag e to the glomeruli, interstitial tissues or tubules a. DM b. Pyelonephritis (clo udy or whitish urine output) c. Presence of stones 3. Post-renal Failure obstruc tion in the urine flow a. Tumor in kidney bladder b. Testicular carcinoma c. Cys tolithiasis Other lecture:, refer to brown paper Nursing Dx: imbalance nutrition: LTBR Hepatic Encephalopathy inability of the li ver to convert ammonia to urea that accumulates causing neurologictoxic manifest ations causes: o liver cirrhosis o hepatitis o Pancreatitis o gallstones ammonia (crosses the BBB blood brain barrier) CHON AA Intestine thru E coli Ammonia Liv er Urea Kidneys Ammoniacal odor of the urine Management admin enemas c intestina l antibiotics eg. Aminoglycosides gentamicin and lactulose (increases the osmola lity incr fluid soft stool attracts the fluids to feces, absorbs NH4 to be dispo sed in the feces) as ordered restrict dietary CHON in the diet: provide a high C HO intake and Vit K supplements RYAN M. ECUNAR, SLU SN IV Saint Louis University College of Nursing Baguio City