Acute Biologic Crisis PDF

ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM abnormal hormone concentrations may also be ca...

ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM abnormal hormone concentrations may also be caused by hormone-producing tumors (aenomas) A ACUTE BIOLOGIC CRISIS located at a remote site a condition that may result to patient mortality if left B3 PHYSICAL EXAMINATION unattended for a brief period of time a condition that warrants immediate attention for the objective findings may be obvious and related to the reversal of disease process and prevention of further patients complaints or may be “silent signs” of which morbidity or mortality the patient is completely unaware thorough physical examination of all body systems, particularly the integumentary, cardiovascular and B ENDOCRINE SYSTEM REVIEW neurologic systems may reveal key findings of endocrine system is a network of glands and organs endocrine dysfunction that produce, store and secrete hormones regulate numerous body functions, including C GLANDS metabolism, growth and development tissue function and mood endocrine = directly into the bloodstream endocrine works in conjunction with the nervous exocrine = sweat glands which secretes their products system to maintain homeostasis through ducts onto epithelial surfaces or into the GI tract pancreas = both endocrine and exocrine B1 GENERAL EFFECTS OF HORMONE endocrine system uses chemical messengers called ACTION hormones to regulate a range of bodily functions regulate the overall metabolic rate and the storage, through the release of hormones conversion and release of energy ○ the hormones then tell these organs and ○ metabolic rate = thyroid gland tissues what to do and how to function regulate fluid and electrolyte balance ○ adrenal gland C1 HYPOTHALAMUS initiating coping responses to stressors regulate growth and development Hypothalamus - produces multiple hormones that ○ pituitary gland and thyroid gland control the pituitary gland regulate reproduction processes ○ sleep-wake cycle ○ Gonads ○ body temperature ○ Appetite ○ regulate the function of other endocrine B2 REGULATION OF HORMONES glands hormone secretion is typically controlled through ○ growth hormone releasing hormone - negative feedback system regulates growth hormone release in the ○ fall in blood concentration of hormone leads pituitary gland to activation of the regulator endocrine gland ○ thyrotropin releasing hormone - TSH and to release of it stimulator hormones release in the pituitary gland ○ elevations in blood concentration of target ○ gonadotropin releasing hormone - cell hormones or of changes in blood regulates LH/FSH production in the pituitary composition resulting from target cell activity gland can cause inhibition of hormone secretion ○ corticotropin releasing hormone - Endocrine disorders are manifested as states of adenocorticortopin release in the pituitary hormone deficiency or hormone excess. The gland underlying pathophysiology may be expressed as: ○ primary - the secreting gland releases C2 PITUITARY GLAND inappropriate hormone because of the disease of the gland itself pituitary - below the hypothalamus ○ secondary - the secreting gland releases ○ growth and reproduction abnormal amounts of hormone because of ADH Vasopressin - affects water retention in the disease in a regulator gland (eg pituitary) kidneys; control blood pressure ○ tertiary -the secreting gland releases ACTH adrenocorticotropic hormones - control inappropriate hormone because of production of sex hormones and the production of ○ hypothalamic dysfunction, resulting in eggs and sperm abnormal stimulation by the pituitary gland Growth Hormone - affects growth and development, stimulates protein production, affects fat distribution PAGE 1 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM Luteinizing hormone and FSH - control production of hormone of sex hormone and production of eggs C8 PANCREAS and sperms Oxytocin - contraction of uterus of uterus and milk Pancreas - located in the abdomen behind stomach ducts in the breast ○ controlling blood sugar level prolactin ○ glucagon - raises blood sugar level tsh (thyroid stimulating hormone) ○ insulin - lowers blood sugar level; stimulates metabolism of glucose, protein and fat C3 PINEAL GLAND C9 KIDNEY pineal - middle of the brain ○ sleep-wake cycles kidney ○ melatonin - released during night hours to ○ renin and angiotensin - controls bp; help with sleep regulating aldosterone production from the Melatonin adrenal gland ○ erythropoietin - affects RBC production C4 THYROID GLAND C10 GONADS thyroid - front part of the neck ○ Metabolism Ovaries ○ thyroid hormone - control metabolism ○ estrogen - affects development of female affects growth, maturation and nervous sexual characteristics and reproductive system activity development ; function of uterus and breasts ○ T3 - triiodothyronine ; bone health ○ T4 - thyroxine ○ progesterone - stimulates the lining of the uterus for fertilization; prepares breast for milk production C5 PARATHYROID GLAND Testes ○ Testosterone -develop and maintain male parathyroid gland – front of the neck sexual characteristics and maturation ○ maintaining control of calcium levels in the bones and blood parathyroid hormone - most important regulator of D COMMON SILENT SIGNS ASSOCIATED blood calcium level WITH ENDOCRINE DISORDERS C6 THYMUS D1 THYROID DYSFUNCTION thymus - upper torso ; active until puberty unexplained weight changes - unexplained weight ○ hormones important for the development of a gain or weight loss without changes in diet could type of WBC called T-cell indicate problems of the thyroid gland ○ Humoral factors- help develop lymphoid fatigue and weakness - persistent tiredness and system muscle weakness can be signs of hypothyroidism and hyperthyroidism C7 ADRENAL hair and skin changes - dry, brittle hair and skin (hypo) or thinning hair and moist smooth skin (hyper) Adrenal - top of each kidney cold and heat intolerance - feeling unusually cold ○ blood pressure (hypo) or hot (hyper) ○ heart rate mood changes - depression (hypo) ○ stress response aldosterone - regulates salt, water balance and blood pressure D2 DIABETES MELLITUS corticosteroid - acts as an anti-inflammatory, increased thirst and urination - polydipsia and maintains blood sugar levels, blood pressure and polyuria muscle strength; regulates salt and water balance blurred vision - high blood sugar levels can affect the epinephrine - increase heart rate, oxygen intake and lens of the eyes blood flow slow healing sores - poor wound healing may norepinephrine - maintains blood pressure indicate high blood sugar levels PAGE 2 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM frequent infections - recurrent infections such as UTI or skin infection E DIAGNOSTIC TESTS numbness or tingling - peripheral neuropathy, especially in the hands and feet E1 THYROID PROBLEMS D3 ADRENAL DYSFUNCTION TSH - thyroid stimulating hormone - tsh a hormone made in pituitary glands unexplained weight gain - particularly around the t4 thyroxine - a high blood level of t4 may mean abdomen and face (Cushing’s syndrome) hyper. a low of t4 may mean hypo fatigue and muscle weakness - persistent tiredness ○ In some cases, high or low t4 levels may not and muscle weakness (addison’s disease or adrenal mean that there are thyroid problems. insufficiency pregnancy or taking of oral contraceptives, skin changes - hyperpigmentation or darkening of makes thyroid hormone levels higher the skin especially in the sin folds (Addison's disease) t3 triiodothyronine - if the health care professional salt cravings - intense craving for salty foods can thinks a patient may have hyperthyroidism even indicate adrenal insufficiency though his t4 level is normal, he may order for t3 test low blood pressure to confirm the diagnosis ○ sometimes t4 D4 PARATHYROID DYSFUNCTION thyroid antibody test These antibodies are used to detect the bone pain and fractures - increased risk of fractures presence of antibodies that target the thyroid and bone pain (hyper) gland. these antibodies can indicate an muscle cramps and spasms - tetanus and muscle autoimmune disorder affecting the thyroid cramps due to low calcium levels (hypo) gland, where the body’s immune system fatigue and weakness - general feeling of tiredness mistakenly attacks the thyroid gland and weakness (hyper) depression and memory issue - gobioid changes, fine needle aspiration (FNA) biopsy of the thyroid including depression and memory problems,s (hyper) ○ When an ultrasound shows a thyroid nodule, an FNA biopsy is often the next step. your doctor takes a sample of the nodule using a D5 PITUITARY DYSFUNCTION thin needle ○ there’s little pain with this test, though we vision changes - loss of peripheral vision or visual offer anesthesia if needed disturbances due to pituitary tumors ○ our lab experts then study the sample under headaches - persistent headaches can be a sign of a microscope to see if it’s cancerous. we’re pituitary tumors often able to give results on the same day growth abnormalities - excessive growth in adults thyroseq genetic test- when FNA biopsy aren’t clear, (acromegaly or children (gigantism) due to excess uses sample growth hormone menstrual irregularities - changes in menstrual cycle or amenorrhea E2 PARATHYROID GLANDS sexual dysfunction calcium level - many conditions can raise calcium levels, but the doctor can diagnose D6 GONADAL DYSFUNCTION hyperparathyroidism if blood tests show a high level of parathyroid hormone infertility - difficulty conceiving could indicate parathyroid hormone tests - increased level hormonal imbalances (low testosterone or polycystic indicates hyper ovary syndrome) blood calcium irregular menstrual cycle - irregular or absent periods can signal hormonal problems hot flashes and night sweats common in E3 ADRENAL GLANDS menopausal women but can also indicate hormonal imbalances acth stimulation test - used most often to diagnose breast changes - unexplained changes in breast adrenal insufficiency. In this test used most often to tissue including tenderness or enlargement in men diagnose adrenal insufficiency. In this test, an (gynecomastia) intravenous (iv) injection of man-made acth, is administered. sample of blood a. insulin tolerance test - an iv injection of the hormone insulin is administered, the dose is high enough to PAGE 3 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM cause hypoglycemia, which causes physical stress, kidney and muscle cells. the increased ammonia and normally triggers the pituitary to make more acth concentration in the blood causes brain dysfunction blood is drawn at the beginning of the test and again and damage, resulting in hepatic encephalopathy every half hour during the next 2 hours ○ diet: high calorie, low protein Circumstances that increase serum ammonia levels tend to aggravate or precipitate hepatic E4 PANCREAS encephalopathy The largest source of ammonia is the enzymatic and fasting blood glucose test bacterial digestion of dietary and blood proteins in a1c test - is a blood test that provides the average the GI tract (low protein, high calorie diet - carbs) levels of blood glucose over the last 3 months. other Ammonia from these sources is increased as a result names for the a1c test are hemoglobin a1c, hba1c, of GI bleeding (ie, bleeding esophageal varices or glycated hemoglobin,and glycosylated hemoglobin chronic GI bleeding), a high-protein diet, bacterial test infections and uremia. ogtt (oral glucose tolerance test) - usually serum ammonia is decreased by elimination of protein prescribed for pregnant women suspected to have from the diet and by the administration of antibiotic gestational diabetes. fast for 8 hours then a high agents, such as neomycin sulfate, that reduce the sugar juice is given, test after 2 hours number of intestinal bacteria capable of converting ○ 140 mg/dl and below is normal mg - dl > x 8 urea to ammonia ○ 140 to 199 impaired glucose tolerance test Other factors unrelated to increased serum ammonia ○ 200 and above indicates diabetes levels that may cause hepatic encephalopathy in susceptible patients include excessive diuresis, A HEPATIC ENCEPHALOPATHY dehydration, infections, surgery, fever, and some medications (sedative agents, tranquilizers, analgesic a life-threatening complication of liver disease, agents, and diuretic medications that cause occurs with profound liver and may result from the potassium loss). accumulation of ammonia and other toxic metabolites Hepatic coma, or hepatic encephalopathy, is a in the blood complex condition resulting from severe liver hepatic coma represents the most advanced stage of dysfunction. The liver’s inability to detoxify harmful hepatic encephalopathy substances, primarily ammonia, leads to a range of some researches describe a false or weak neurological symptoms neurotransmitter as a cause, but the exact mechanism is not fully understood these false neurotransmitters may be generated from A2 ETIOLOGIES an intestinal source and result in the precipitation of Liver Cirrhosis encephalopathy portal-systemic encephalopathy, the most common type of hepatic encephalopathy, occurs primarily in patients with cirrhosis, with portal hypertension and portal systemic shunting A1 PATHOPHYSIOLOGY multifactorial and involves complex interactions between liver dysfunction, accumulation of neurotoxic ○ Description: Cirrhosis is the late stage of substances, and alterations in neurotransmission scarring (fibrosis) of the liver caused by ammonia accumulates because damaged liver cells many forms of liver diseases and conditions, fails to detoxify and convert to urea, the ammonia that such as hepatitis and chronic alcoholism is constantly entering the bloodstream ○ Mechanism: scar tissue replaces healthy ammonia production: ammonia is produced liver tissue, obstructing blood flow through primarily by intestinal bacteria during protein digestion the liver and impairing its ability to detoxify and by the breakdown of amino acids toxins ammonia metabolism: normally, ammonia is Hepatitis converted into urea in the liver through the urea cycle ○ Description: Inflammation of the liver, and secreted by the kidneys typically caused by viral infections (hepatitis Impaired conversion: In liver failure, the urea cycle A, B, C, D, and E), and alcohol use, toxins, is disrupted, leading to elevated levels of ammonia in and certain medications the blood (hyperammonemia) ○ Mechanism: inflammation and liver cell ammonia enters the bloodstream as a result of its damage reduce the liver’s detoxification absorption from the GI tract and its liberation from capacity, leaving to toxin accumulation in the bloodstream PAGE 4 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM Acute Liver Failure ○ Mechanism: Impaired renal function ○ Description: a rapid loss of liver function, decreases the excretion of ammonia and often within days or weeks, usually in a other toxins, leading to their accumulation person without preexisting liver disease ○ Mechanism: sudden liver failure can result from drug toxicity (e.g acetaminophen A3 CLINICAL MANIFESTATION overdose), infections, and other causes The earliest symptoms of hepatic encephalopathy leading to an inability to clear toxins. include minor mental changes and motor Portosystemic shunts disturbances. The patient appears slightly confused, ○ Description: abnormal blood flow patterns has alterations in mood, becomes unkempt, and has that bypass the liver, common in advanced altered sleep patterns liver disease The patient tends to sleep during the day and have ○ Mechanism: Blood carrying toxins from the restlessness and insomnia at night. As hepatic intestines bypasses the liver and directly encephalopathy progresses, the patient may be enters the systemic circulation, resulting in difficult to awaken. high toxin levels in the brain asterixis (flapping tremor of the hands) may occur. Gastrointestinal Bleeding Simple tasks, such as handwriting, become difficult. A ○ Description: bleeding within the handwriting or drawing sample (eg, star figure), taken gastrointestinal tract, often associated with daily, may provide graphic evidence of progression or varices in the esophagus or stomach reversal of hepatic encephalopathy ○ Mechanism: blood in the intestines increases inability to reproduce simple figure referred to as nitrogenous waste, which is converted to constructional apraxia ammonia, exacerbating hepatic In the early stages of hepatic encephalopathy, the encephalopathy deep tendon reflexes are hyperactive; with worsening Electrolyte imbalances of hepatic encephalopathy, these reflexes disappear ○ Description: disturbances on the levels of and the extremities may become flaccid electrolytes such as sodium and potassium ○ Mechanism: imbalances, particularly hyponatremia (low sodium), can affect brain A4 ASSESSMENT AND DIAGNOSTIC function and contribute to the development FINDINGS of hepatic encephalopathy hyponatremia can be caused by the electroencephalogram (ECG) shows generalized SIADH slowing, an increase in the amplitude of brain waves, Infection and characteristic triphasic waves ○ Description: bacterial infections, such as occasionally, fetor hepaticus, a sweet, slightly fecal spontaneous bacterial peritonitis, are odor to the breath presumed to be of intestinal origin common in patients with cirrhosis may be noticed. the odor has also been described as ○ Mechanism: infections can precipitate similar to that of freshly mowed grass acetone, or old hepatic encephalopathy by increasing wine, fetor hepaticus is prevalent with extensive metabolic demands and toxin production collateral portal circulation in chronic kidney disease Dehydration in a more advanced stage, there are gross ○ Description: Insufficient fluid intake or disturbances of consciousness and the patient is excessive fluid loss completely disoriented with respect to time and place, ○ Mechanism: dehydration can lead to with further progression of the disorder the patient electrolyte imbalances, and reduced renal lapses into frank coma and may have seizures clearance of toxins, worsening hepatic Approximately 35% of all patients with cirrhosis of the encephalopathy liver die in hepatic coma Constipation: ○ Description: infrequent bowel movements ○ Mechanism: constipation leads to increased A5 MEDICAL MANAGEMENT intestinal production and absorption of lactulose is administered to reduce serum ammonia ammonia, contributing to higher toxin levels levels. it acts by several mechanisms that promote Medications the excretion of ammonia in the stool: ○ Description: use of certain medications such ○ (1) ammonia is kept in an ionizes state, as sedatives, tranquilizers, and diuretics resulting in a fall of colon pH, reversing the ○ Mechanism: These medications can depress passage of ammonia from the colon of the central nervous system function or lead to blood electrolyte imbalances, exacerbating hepatic ○ (2) evacuation of the bowel takes place, encephalopathy which decreases the ammonia absorbed by Renal Dysfunction the column ○ Description: kidney dysfunction or failure PAGE 5 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM ○ The fecal flora are changes to organisms the nurse is responsible for maintaining a safe that do not produce ammonia from urea environment to prevent injury, bleeding and infection. ○ two or three soft stools per day are THe nurse administers the prescribed treatments and desirable; this indicates that lactulose is monitors that patient for the many potential performing as intended complications. The nurse also communicates with the ○ Possible side effects include intestinal patient’s family to keep them informed about the bloating and cramps, which usually patient’s status, and supports them by explaining the disappear within a week. To mask the sweet procedures and treatments that are part of the taste, to which some patients object, patient’s care. lactulose can be diluted with fruit juice. ○ NEVER the prognosis ○ The patient is closely monitored for if the patient recovers from hepatic encephalopathy hypokalemia and dehydration and coma, rehabilitation is likely to be prolonged. ○ Other laxatives are not prescribed during Thus, the patient and family will require assistance to lactulose administration because their effects understand the causes of this severe complication would disturb dosage regulation. and to recognize that it may recur ○ lactulose can be administered by nasogastric tube or enema for patients who are comatose or in whom oral administration is A7 NURSING DIAGNOSES contraindicated of impossible 1. Ineffective Breathing Pattern (Ineffective breathing other aspects of management include iv pattern related to decreased level of consciousness administration of glucose to minimize protein and respiratory muscle weakness) breakdown, administration of vitamins to correct ○ Respiratory Monitoring: Monitoring rate, deficiencies, and correction of electrolyte imbalances depth and effort (especially potassium) ○ Positioning: Position the patient to additional principles of management of hepatic maximize respiratory function, such as encephalopathy include the ff: elevating the head of the bed ○ Therapy is directed toward treating or ○ Oxygen Therapy: Administer oxygen as removing the cause prescribed. ○ neurologic status is assessed frequently. A ○ Airway Management: Be prepared to daily record is kept of handwriting and manage the airway and provide suctioning if performance in arithmetic to monitor mental the patient is unable to clear secretions status ○ fluid intake and output of the body weight are 2. Fluid Volume Deficit (Fluid volume deficit related to recorded each day vomiting, diarrhea (from lactulose), or decrease oral ○ vital signs are measured and recorded every intake 4 hours ○ IV Fluids: administer intravenous fluids as ○ potential sites of infection (perineum, lungs) prescribed to maintain hydration are assessed frequently, and abnormal ○ Monitor Output: Monitor intake and output findings are reported promptly accurately to assess fluid balance ○ serum ammonia level is monitored daily ○ Electrolyte Monitoring: Monitoring ○ Protein intake is restricted only in patients electrolytes regularly and replace as who are comatose or who have necessary to prevent imbalances encephalopathy that is refractory to lactulose ○ Encourage Oral Intake: Encourage oral and antibiotic therapy fluids as tolerated, unless contraindicated ○ Reduction in the absorption of ammonia from 3. Imbalanced nutrition: Less than Body the GI tract is accomplished by the use of Requirements (related to anorexia, nausea, and gastric suction, enemas, or oral antibiotics. vomiting) ○ Electrolyte status is monitored and corrected ○ dietary consult: consult with a dietician to if abnormal. develop a nutrition plan tailored to the ○ sedatives, tranquilizers, and analgesic patient’s needs medications are discontinued ○ small, frequent meals: offer small, frequent ○ Benzodiazepine antagonists such as meals that are high in calories and protein flumazenil (Romazicon) may be unless contraindicated administered to improve encephalopathy, ○ Nutrition Supplements: Provide nutritional whether or not the patient has previously supplements if the patient is unable to taken benzodiazepines. consume adequate calories and nutrients through regular meals ○ Monitor intake: keep track of the patient’s A6 NURSING MANAGEMENT daily caloric intake and weight PAGE 6 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM 4. Altered Mental Status (related to the accumulation of Teaching Patient Self Care toxins (such as ammonia) in the bloodstream ○ If the patient has recovered from hepatic secondary to liver dysfunction) encephalopathy and is discharged home, the ○ Monitor neurological status: regularly nurse instructs the family to watch for subtle assess the patient’s level of consciousness, signs of recurrent encephalopathy orientation, and behavior ○ In the acute phase of hepatic ○ Ammonia levels: monitor serum ammonia encephalopathy, dietary protein may be levels as ordered reduced to 0.8 to 1.0 g/kg per day. During ○ Lactulose administration: Administer recovery. adnm in the home situation, it is lactulose as prescribed to help reduce important to instruct the patient in ammonia levels. Monitor for diarrhea, which maintaining a low protein, high calorie diet indicate an effective dosage but also risk of ○ Protein may be then added in 10-g dehydration increments every 3-5 days. ○ Safety measures: Implement safety ○ Any relapse is treated with a return to the measures to prevent injury due to confusion previous level or disorientation, such as side rails and a ○ Continued use of lactulose in the home bed alarm environment is not uncommon, and the ○ Family Education: Educate family members patient and family should monitor its efficacy about the condition, expected behaviors, and and side effects closely. Use of vegetable safety precautions rather than animal protein may be indicated 5. Impaired Skin Integrity (related to immobility and in patients those daily protein tolerance is poor nutritional status) less than 1g/kg ○ skin assessment: perform regular skin ○ Vegetable protein intake may result in assessments to identify early signs of improved nitrogen balance without breakdown precipitating or advancing hepatic ○ repositioning: reposition the patient every 2 encephalopathy hours to prevent pressure ulcers Continuing Care ○ skin care: keep the skin clean and dry. use ○ Referral for home care is warranted for the barrier creams to protect the skin from patient whose returns home after recovery incontinence from hepatic encephalopathy ○ specialty mattress: utilize a ○ The home care nurse assesses the patient’s pressure-relieving mattress if necessary (egg physical and mental status and collaborates crate mattress) closely with the physician. The home visit 6. Risk for Injury (related to altered level of also provides an opportunity for the nurse to consciousness and impaired judgment) assess the home environment and the ability ○ Fall precautions: implement fall precautions of the patient and family to monitor signs and such as keeping the bed in the lowest symptoms and to follow the treatment position and ensuring the environment is free regimen. from hazards ○ Home care visits are particularly important if ○ Supervision: Provide close supervision, the patient lives alone, because especially during periods of agitation or encephalopathy may affect the patient’s confusion ability to remember or follow the treatment ○ Restraints: use restraints only as a last regimen. resort and according to hospital policy ○ The nurse reinforces previous teaching and 7. Risk for Infection (related to compromised immune reminds the patient and family about the function and invasive procedures) importance of dietary restrictions, close ○ Hand hygiene: strict adherence to hand monitoring, and follow-up hygiene protocols ○ Aseptic Technique: Use aseptic technique B DIABETIC KETOACIDOSIS (DKA) for invasive procedures ○ Monitor for infection: Regularly monitor for is caused by an absence or markedly inadequate signs and symptoms of infection, such as amount of insulin. This deficit in available insulin fever, redness or discharge from invasive results in disorders in the metabolism of sites carbohydrates, protein and fat ○ Patient education: Educate the patient and Three main clinical features of DKA are as follows” family about infection prevention measures. ○ hyperglycemia ○ dehydration (diarrhea, n&v, temp extremes) and electrolyte loss A8 PROMOTING HOME AND ○ acidosis COMMUNITY-BASED CARE PAGE 7 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM coping with diabetes or other aspect in their lives), or B1 SYMPTOMS equipment problems (e.g. occlusion of insulin pump tubing) Illness and infections are associated with insulin resistance. In response to physical (and emotional) stressors, there is an increase in the level of “stress” hormones — glucagon, epinephrine, norepinephrine, cortisol, and growth hormone. These hormones promote glucose production by the liver and interfere with glucose utilization by muscle and fat tissue, counteracting the effect of insulin If insulin levels are not increased during times of illness and infection, hyperglycemia may progress to DKA B3 PREVENTION For prevention of DKA related to illness, “sick day B2 PATHOPHYSIOLOGY rules” for managing diabetes when ill, should be reviewed with patients. Insulin moves glucose from your blood into cells all The most important concept in this is to never over your body. eliminate insulin doses when nausea and vomiting Without insulin, the amount of glucose entering the occur. cells is reduced, and the production and release of Instead, the patient should take the usual insulin dose glucose by the liver (gluconeogenesis) are (or previously prescribed special sick day doses) and increased, leading to hyperglycemia. then attempt to consume frequent small portions of In an attempt to rid the body of the excess glucose, carbohydrates the kidneys excrete the glucose along with water and This include foods usually avoided, such as juices, electrolytes (e.g. sodium and potassium). This regular sodas, and gelatin osmotic diuresis, which is characterized by excessive Drinking fluids every hour is important to prevent urination (polyuria), leads to dehydration and marked dehydration. Blood glucose and urine ketones must electrolyte loss be assessed every 3 to 4 hours Patients with severe DKA may lose up to 6.5L of water and up to 400-500 mEq of sodium, potassium, and chloride over a 24-hour period. Another effect of B4 GUIDELINES DURING PERIODS OF insulin deficiency or deficit is the breakdown of ILLNESS “SICK DAY RULES” fat (lipolysis) into free fatty acids and glycerol. The free fatty acids are converted into ketone bodies the nurse instructs the patient to: by the liver. Ketone bodies are acids; their ○ take insulin or oral antidiabetic agents as accumulation in the circulation due to lack of insulin usual leads to metabolic acidosis metformin Three main causes of DKA are decreased or missed ○ test blood glucose and urine ketones every dose of insulin, illness or infection, and undiagnosed 3-4 hours and untreated diabetes (may be the first manifestation ○ report elevated glucose levels are specified of type 1 diabetes). An insulin deficiency may result or urine ketone to your primary provider from an insufficient dosage of insulin prescribed or ○ take supplemental doses of regular insulin from insufficient insulin being given by the patient every 3 to 4 hours. If needed, if you take Errors in insulin dosage may be made by patients insulin who are ill and who assume that they are eating less ○ substitute soft foods (e.g., ⅓ cup regular or if they are vomiting, they must decrease their gelatin, 1 cup cream soup, ½ cup custard, 3 insulin doses. squares graham crackers) six to eight times Because illness, especially infections, can cause a day if you cannot follow your usual meal increased blood glucose levels, the patient does not plan need to decrease the insulin dose to compensate for ○ Take liquids (e.g. ½ cup regular cola or decreased food intake when ill and may even need to orange juice, ½ cup broth, 1 cup sports drink increase the insulin dose. [gatorade] every ½ to 1 hour to prevent other potential causes of decreased insulin include dehydration and provide calories if vomiting, patient error in drawing up or injecting insulin diarrhea, or fever persists. (especially in patient with visual impairments), ○ report nausea, vomiting, and diarrhea, to intentional skipping of insulin doses (especially in your primary provider, because extreme fluid adolescents with diabetes who are having difficulty loss may be dangerous PAGE 8 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM ○ be aware that if you are unable to retain oral The severity of DKA is not necessarily related to fluids, you may require hospitalization to blood glucose levels. Evidence of ketoacidosis is avoid diabetic ketoacidosis and possibly reflected in low serum bicarbonate (0-15 mEq/L) and coma low pH (6.8-7.3) values. ○ if the patient cannot take fluids without A low partial pressure of carbon dioxide (PCO2 10 to vomiting, or if elevated glucose or ketone 30 mmHg) reflects respiratory compensation levels persist, the provider must be (Kussmaul respirations) for the metabolic acidosis. contacted accumulation of ketone bodies (which precipitates the ○ Patients are taught to have foods available acidosis) is reflected in blood and urine ketone for use on sick days. In addition, a supply of measurements urine test strips (for ketone testing) and sodium and potassium concentration may be low, blood glucose test strips should be available. normal, or high depending on the amount of water ○ The patient must know how to contact their loss (dehydration). Despite the plasma concentration, primary provider 14 hours a day. These there has been a marked total body depletion of these materials should be assembled in a “sick (and other) electrolytes, and they will need to be day” kit replaced. ○ After the acute phase of DKA has resolved, Increased levels of creatinine, blood urea nitrogen the nurse should assess for underlying (BUN), and hematocrit may also be seen with causes. If there are psychological reasons dehydration. After rehydration, continued elevation in for the patient missing insulin doses, the the serum creatinine and BUN levels suggests patient and family may be referred for underlying renal insufficiency evaluation and counseling or therapy B7 MANAGEMENT B5 CLINICAL MANIFESTATIONS In addition to treating hyperglycemia, management of The hyperglycemia of DKA leads to polyuria, DKA is aimed at correcting dehydration, electrolyte polydipsia (increased thirst), and marked fatigue. In loss, and acidosis before correcting the addition, the patient may experience blurred vision, hyperglycemia with insulin. weakness, and headache. Patients with marked 1. Rehydration intravascular volume depletion may have orthostatic ○ In dehydrated patients, rehydration is hypotension (drip in systolic blood pressure of 20 important for maintaining tissue perfusion. In mmhg or more on changing from a reclining to a addition, fluid replacement enhances the standing position) excretion for excessive glucose by the volume depletion may also lead to frank hypotension kidneys. The patient may need as much as 6 with a weak, rapid pulse to 10 L of IV fluid to replace fluid losses The ketosis and acidosis of DKA lead to caused by polyuria, hyperventilation, gastrointestinal symptoms such as anorexia, nausea, diarrhea or vomiting vomiting, and abdominal pain. ○ Initially, 0.9% sodium chloride (normal saline The patient may have acetone breath (fruity odor), [NS]) solution is given at a rapid rate, usually which occurs with elevated ketone levels. In addition, 0.5 to 1 L per hour for 2 to 3 hours. Half hyperventilation (with very deep, but not labored, strength NS (0.45%) solution (also known as respirations) may occur hypotonic saline solution) may be used for these kussmaul's respirations represent the body’s patients with hypertension or hypernatremia attempt to decrease the acidosis, counteracting the and those at risk for heart failure effect of the ketone buildup ○ after the first few hours, half-strength NS Kussmaul breathing is characterized by deep, rapid, solution is the fluid of choice for continued and labored breathing. rehydration, provide the blood pressure is certain medical conditions, such as DKA, which is a stable and the sodium level is low serious complication of diabetes ○ moderate to high rates of infusion (200 to In addition, mental status in DKA varies widely. the 500mL per hour) may be needed for several patient may be alert, lethargic, or comatose more hours. When the blood glucose level reaches 300 mg/dL (16.6mmol/L) or less, the Iv solution may be changes to dextrose 5% B6 ASSESSMENT AND DIAGNOSTIC in water (D5W) to prevent a precipitous FINDINGS decline in the blood glucose level Blood glucose levels may vary between 300 and 800 ○ Monitoring of fluid volume status involves mg/dL (16.6 and 44.4 mmol/L). Some patients have frequent measurements of vital signs lower glucose values, and others have values of 1000 (including monitoring for orthostatic changes mg/dL (55.5 mmol/L) or higher (usually depending on in blood pressure and heart rate), lung the degree of dehydration PAGE 9 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM assessment and monitoring of intake and rapid drop in the blood glucose level (i.e., output. hypoglycemia) during treatment ○ Initial urine output lags behind IV fluid intake ○ Regular insulin, the only type of insulin as dehydration is corrected. Plasma approved for IV use, may be added to IV expanders may be necessary to correct solutions severe hypotension that does not respond to ○ The nurse must convert hourly rates of IV fluid replacement. insulin infusion (frequently prescribed as ○ monitoring for signs of fluid overload is units per hour) to IV drip rates. For example, especially important for patients who are if 100 units of regular insulin are mixed into older, have renal impairment or are at risk for 500 mL of 0.9 NS, then 1 unit of insulin heart failure equals 5 mL; therefore, an initial insulin 2. Restoring Electrolytes infusion rate of 5 units per hour would equal ○ The major electrolyte concern during 25 mL per hour. treatment of DKA is potassium. The initial ○ the insulin is often infused separately from plasma concentration of potassium may be the rehydration solutions to allow frequent low, normal, or high, but more often than not, changes in the rate and content of the latter tends to be high (hyperkalemia) from ○ Insulin must be infused continuously until disruption of the cellular sodium-potassium subcutaneous administration of insulin can pump (in the face of acidosis). be resumed. ANy interruption in ○ Therefore, the serum potassium level must administration may result in the be monitored frequently. some of the factors reaccumulation of ketone bodies and related to treating DKA that affect potassium worsening acidosis concentration include rehydration, which ○ Even if blood glucose levels are decreasing leads to increased plasma volume and and returning to normal, the insulin drip must subsequent decreases in the concentration not be stopped until subcutaneous insulin of serum potassium therapy has been started. ○ rehydration also leads to increased urinary ○ rather, the rate or concentration of the excretion of potassium. Insulin administration dextrose infusion may be increased to enhances the movement of potassium from prevent hypoglycemia. blood glucose levels the extracellular fluid into the cells. are usually corrected before the acidosis is ○ cautious but timely potassium replacement is corrected vital to avoid dysrhythmias that may occur ○ Therefore IV insulin may be continued for 12 with hypokalemia to 24 hours, until the serum bicarbonate level ○ as much as 40 mEq per hour may be increases (to at least 15 to 18 mEq/L) nad needed for several hours. because until the patient can eat extracellular potassium levels decrease ○ In general, bicarbonate infusion to correct during DKA treatment, potassium must be severe acidosis is avoided during treatment infused even if the plasma potassium level is of DKA because it precipitates further, normal sudden (and potentially fatal) decreases in ○ frequent (every 2 to 4 hours initially) ECGs serum potassium levels. and laboratory measurements of potassium ○ continuous insulin is usually sufficient for are necessary during the first 8 hours of reversal of DKA (Noble-Bell & Cox, 2014; treatment. Potassium replacement is Umpeirrez & Korykowski, 2016) withheld only if hyperkalemia is present or if the patient is not urinating. 3. Reversing Acidosis ○ ketone bodies (acids) accumulate as a result B8 NURSING DIAGNOSES WITH of fat breakdown. The acidosis that occurs in INTERVENTIONS DKA is reversed with insulin, which inhibits 1. Ineffective Breathing Pattern fat breakdown,thereby ending ketone ○ Assessment production and acid buildup. Insulin is monitor respiratory depth usually infused at a slow, continuous rate assess for signs of respiratory (e.g. 5 units per hour) distress (e.g., Kussmaul foods: calories from fat, respirations carbohydrate ○ Interventions: ○ Hourly blood glucose values must be Administer oxygen as needed measured. IV fluid solutions with higher Position pt to facilitate optimal concentrations of glucose, such as NS breathing )semi fowlers) solution )eg D5NS, D5.45NS), are given Monitor Arterial Blood Gasses when blood glucose levels reach 250 to 300 2. Electrolyte Imbalance mg/dL (138 to 16.6 mmol/L) to avoid too PAGE 10 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM ○ Assessment keep emergency equipment readily Monitor serum electrolyte levels available (potassium, sodium, chloride 7. Knowledge Deficit observe for signs of electrolyte ○ assessment imbalances (e.g. muscle cramps, Assess the patient’s understanding arrhythmias) of DKA and diabetes management ○ Intervention identify any gaps in knowledge administer electrolytes as ○ interventions prescribed, particularly provide comprehensive education Educate the patient on the on diabetes management including importance of maintaining insulin administration, diet, and electrolyte balance exercise 3. Deficient Fluid Volume teach the patient how to monitor ○ Assessment blood glucose levels and recognize monitor vital signs, especially blood symptoms of DKA pressure and heart rate provide written materials and check for signs of dehydration (e.g. resources for further education dry mucous membranes, decreased skin turgor) ○ intervention C THYROID CRISIS/ ADRENAL CRISIS administer IV fluids (usually isotonic Thyroid storm or thyroid crisis is a life threatening saline initially) event that occurs in patients with uncontrolled Monitor intake and output hyperthyroidism and occurs most often with Graves’ Assess for signs of fluid overload disease (an autoimmune system disorder that causes (e.g edema, crackles in lungs) an overactive thyroid gland). Manifestations develop 4. Imbalanced Nutrition: Less than Body quickly. It is often triggered by stressors such as Requirements trauma, infection, diabetic ketoacidosis, and ○ assessment pregnancy. monitor blood glucose levels other conditions that can lead to thyroid storm include frequently vigorous palpation of the goiter, exposure to iodine, assess for signs of malnutrition or and radioactive iodine (RAI) therapy weight loss ○ RAI - done to pt with hyperthyroidism ○ interventions ○ consideration: no exposure / contact for at administer insulin as prescribed least a week after RAI therapy (isolation) provide small, frequent meals if tolerated and appropriate monitor blood glucose levels and adjust insulin doses accordingly 5. Risk for Infection ○ assessment monitor for signs of infection (e.g. fever, redness, swelling) perform regular skin assessments ○ intervention Practice aseptic techniques during IV insertion and other procedures Educate the patient on proper Although thyroid storm after surgery is less common hygiene practices because of drug therapy before thyroid surgery, it can Administer antibiotics as prescribed still occur. if infection is present The manifestations of thyroid storm are caused by 6. Risk for Injury excessive thyroid hormone release, which ○ assessment dramatically increases metabolic rate. Assess for changes in mental Key manifestations include fever, tachycardia and status or level of consciousness systolic hypertension. The patient may have monitor for signs of hypoglycemia abdominal pain, nausea, vomiting and diarrhea. Often ○ interventions he or she is very anxious and has tremors. As the maintain a safe environment to crisis progresses, the patient may become restless, prevent falls or injury confused or psychotic and may seizures, leading to educate the patient and family on coma recognizing symptoms of even with treatment, thyroid storm may lead to death hypoglycemia and hyperglycemia PAGE 11 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM Thyroid storm can occur in Graves disease (more C1 CRITICAL RESCUE common), toxic adenoma, and multinodular toxic When caring for a patient with hyperthyroidism, even goiter after a thyroidectomy, immediately report a Mortality/Morbidity fatal when untreated temperature increase of even 1 degree F because it ○ mortality is between 20-30% may indicate an impending thyroid crisis. Emergency measures to prevent death vary with the C4 SIGNS AND SYMPTOMS intensity and type of manifestations. Interventions focus on maintaining airway patency, providing adequate ventilation, reducing fever and stabilizing the hemodynamic status Uncomplicated Thyroid Storm Thyrotoxicosis C2 EMERGENCY CARE FOR THE PATIENT Heat Intolerance, hyperpyrexia, temperature in DURING THYROID STORM diaphoresis excess of 106 degrees celsius, dehydration Maintain a patent airway and adequate ventilation Give oral antithyroid drugs as prescribed: methimazole ( Tapazole), up to 60 mg daily; Sinus Tachycardia, Heart heart rate faster than 140 propylthiouracil (PTU, Propyl-Thyracil), 300 to 900 rate 100-140 bpm, hypotension, atrial mg daily. dysrhythmias, congestive Administer sodium iodide solution 2g IV daily as heart failure prescribed Give propranolol (Inderal, Detensol), 1 to 3 mg IV as Diarrhea, increased appetite nausea, vomiting, severe prescribed. Give slowly over 3 mins. The pt should be with loss of weight diarrhea, abdominal pain, connected to a cardiac monitor, and central venous hepatocellular pressure catheter should be in place dysfunction-jaundice Give glucocorticosteroids as prescribed: hydrocortisone, 100 to 500 mg IV daily; prednisone, 4 Anxiety, restlessness confusion, agitation, to 60 mg IV daily; or dexamethasone, 2 mg IM every delirium, frank psychosis, 6 hrs seizure, stupor or coma ○ glucocorticoids - help in metabolism & reduce inflammation Monitor continually for cardiac dysrhythmias Unusual Presentations ○ monitor vital signs every 30 mins ○ Chest pain ○ provide comfort measures, including cooling ○ acute abdomen blanket ○ status epilepticus ○ give non salicylate antipyretics as prescribed ○ stroke epilepticus ○ correct dehydration with normal saline ○ acute renal failure due to rhabdomyolysis infusions ○ apathetic hypothyroidism (masked ○ apply cooling blanket or ice packs to reduce hyperthyroidism) present without goiter, fever ophthalmopathy, or prominent symptoms of hyperthyroidism. These patients have a low pulse rate and a propensity to develop C3 THYROID CRISIS (CONT..) thyroid storm, due to delay in diagnosis a clinical manifestation of an extreme hyperthyroid state which may lead to disability and death. C5 PATHOPHYSIOLOGY Before, Thyroid storm is a common complication of toxic goiter surgery, may occur during intraoperative Hyperthyroid state + precipitating factor → increase in or postoperative. thyroid hormone (shift from protein bound to free Today it is more commonly seen in a thyrotoxic hormone) → sudden increase in metabolism → patient with an intercurrent illness or surgical exaggerated signs and symptoms of hyperthyroidism emergency. Who are untreated or who were → end organ damage. inadequately treated. Predisposing Factors Early recognition and prompt intervention are ○ some causes that rapidly increase the necessary to manage this phenomenon thyroid hormone levels include the following: Exact Etiology is unknown, precipitating factor surgery, thyroidal or nonthyroidal radioiodine usually found with thyroid storm are: therapy, withdrawal of antithyroid drug ○ Stress (most common), concurrent illness therapy, vigorous thyroid palpation, Iodinated e.g sepsis and surgical emergency contrast dye, Thyroid hormone injections PAGE 12 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM assess creatinine levels before ○ Esmolol - ultra short acting beta-blocking performing CT scan with dye agent used successfully in thyrotoxicosis and ○ Other common precipitating factors thyroid storm include the following: infection, emotional ○ Guanethidine or reserpine given to patients stress, tooth extraction, diabetic with congestive cardiac failure, ketoacidosis, hypoglycemia, trauma, bowel bronchospasm, or history of asthma infarction, parturition (childbirth), toxemia of Supportive Measure pregnancy, pulmonary embolism, ○ aggressive fluid therapy and electrolyte cerebrovascular accident, and gestational therapy: trophoblastic disease. needed for dehydration and hypotension fluid requirements may increase to C6 MANAGEMENT 3-5 L/day Management is a multi-step process ○ invasive monitoring is advisable ○ Ideal Therapy: block the synthesis, ○ vasopressor agents can be used when secretion, and peripheral action of the hypotension persist following adequate fluid thyroid hormone replacement Supportive Therapy ○ add glucose to IV fluids for nutritional ○ stabilize homeostasis support multivitamins especially vitamin B1 ○ reverse multiorgan decompensation are added to prevent Wernicke ○ identify and treat the precipitating factor encephalopathy ○ definitive treatment: avoid recurrence ○ Hyperthermia is treated through central Blocking Thyroid Hormone Synthesis cooling and peripheral heat dissipation ○ Antithyroid Compounds ○ Acetaminophen is a drug of choice, aspirin Propylthyrouracis (PTU) - also may displace thyroid hormone from binding blocks peripheral conversion of T4 sites and increase severity of thyroid storm to T3 and hence it is preferred in ○ cooling blankets, ice packs, and alcohol thyroid storm over MMI sponges encourage dissipation of heat methimazole (MMI) PTU and MMI ○ Glucocorticoids is associated with improved block the incorporation of iodine survival rates due to reduce iodine uptake intro thyroglobulin within 1 hour of ○ Reduce antibody titers of thyroid-stimulating ingestion antibodies with stabilization of the vascular a history of hepatotoxicity or bed agranulocytosis from previous ○ stress dose of glucocorticoid (e.g. thionamide therapy precludes use hydrocortisone, dexamethasone) is routine of PTU and MMI Digitalization required to control the ventricular rate Blocking Thyroid Hormone Secretion in patients with atrial fibrillation ○ Lugol Solution or saturated solution of ○ anticoagulation drugs may be needed for potassium iodide atrial fibrillation and can be administered in ○ iodine therapy should be administered after the absence of contraindications approximately 1 hour following ex. Clopidogrel administration of PTU or MMI ○ congestive cardiac failure may require ○ iodine used alone helps to increase thyroid swan-ganz catheter monitoring hormone stores and may increase thyroid state C7 LABORATORY STUDIES ○ lithium intolerant to iodine no specific diagnostic criteria to establish the unable to take PTU or MMI diagnosis of thyroid storm exist Management Burch and Wartofsky constructed an excellent clinical Blocking Peripheral Action of Thyroid Hormone diagnostic point scale to facilitate a semiquantitative ○ Propranolol: distinction between uncomplicated thyrotoxicosis, drug of choice to counter peripheral impending storm, and established thyroid storm action of thyroid hormone Laboratory findings in thyroid storm are consistent blocks beta-adrenergic receptors with those of thyrotoxicosis and include the following: prevents conversion of T4 to T3 ○ elevated T3 and T4 levels produces dramatic improvement in ○ elevated T3 uptake clinical status and greatly ○ suppressed TSH levels ameliorates symptoms ○ elevated 24 hour radioiodine uptake PAGE 13 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM elevated T4 and decreased TSH are the only myxedema is also used to describe the dermatologic abnormal findings needed for confirmation of changes that occur in hypothyroidism which refers to thyrotoxicosis. deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area It is the deficiency of thyroid hormone resulting in: ○ slowed body metabolism ○ decreased heat production ○ decreased oxygen consumption by tissues D1 RISK FACTORS Chronic autoimmune thyroiditis Thyroidectomy underwent radioactive iodine therapy for hyperthyroidism secondary hypothyroidism Poor compliance and lack of knowledge about managing levothyroxine therapy in acute illness Undiagnosed hypothyroidism Infection, exposure to cold temperatures trauma burns cerebrovascular accident, myocardial infarction congestive heart failure treatment should not be withheld any laboratory respiratory acidosis confirmation of hyperthyroidism when thyroid storm is suspected clinically a 2 hour radioiodine uptake is advisable if thyroid D2 PRECIPITATING FACTORS storm is suspected and no past history of hyperthyroidism Medications Other abnormal laboratory values that point toward ○ sedatives, narcotics, amiodarone, rifampin, decompensation of homeostasis include the following: beta blockers ○ increased BUN and creatinine ○ decreased drug metabolism leading to ○ electrolyte imbalance from dehydration, overdosing of medications particularly anemia, thrombocytopenia, and leukocytosis sedatives, hypnotics, abd anesthetic agents ○ hepatocellular dysfunction as shown by can precipitate myxedema coma elevated levels of transaminases, lactate Metabolic disturbances dehydrogenase, alkaline phosphatase, and ○ hypoglycemia, bilirubin ○ hyponatremia, ○ elevated calcium levels ○ acidosis and ○ hyperglycemia ○ hypercapnia D MYXEDEMA COMA D3 PATHOPHYSIOLOGY is a rare life threatening condition. it is the Decreased levels of thyroid hormones → overall decompensated state of severe hypothyroidism in slowing of basal metabolic rate and slowing of body which the patient is hypothermic and unconscious processes → decreases GI motility, bradycardia, the condition occurs most often among elderly women achlorhydria (decreased production of hydrochloric in the winter months and appears to be precipitated acid) , decreased heat production, decreased basal by cold body temperature → increases serum cholesterol and myxedema coma, occasionally called myxedema triglycerides, atherosclerosis, CAD, anemia, vitamin crisis, is a rare life-threatening clinical condition that B12 and folate deficiency → hypothyroidism represents severe hypothyroidism with physiological CVS - cardiac contractility is impaired leading to decompensation reduced stroke volume, low cardiac output, the condition usually occurs in patients with bradycardia, and hypotension. long-standing undiagnosed hypothyroidism and is CNS - brain function is affected by reduction in usually precipitated by infection, cerebrovascular oxygen delivery and subsequent consumption, disease, heart failure, trauma, or drug therapy decreased glucose utilization and reduced cerebral blood flow PAGE 14 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM Pulmonary - hypoventilation due to central levothyroxine sodium with Iv glucose or depression of ventilatory drive with decreased corticosteroids responsiveness to hypoxia and hypercapnia Renal - hyponatremia common in patients with myxedema coma and is caused by increased serum D7 ICU SETTING WITH CONTINUOUS antidiuretic hormone and impaired water excretion CARDIAC MONITORING and reduced GFR due to low cardiac output airway maintenance is crucial, mechanical ventilation GI - malabsorption, impaired peristalsis, paralytic is commonly required during the first 36-48 hours, but ileus. Ascites may occur due to increased capillary some patients require prolonged respiratory support permeability, heart failure, or other mechanisms. for as long as 2-3 weeks gastrointestinal bleeding secondary to an associated Thyroid hormone replacement - controversial, some coagulopathy may occur favor levothyroxine (T4) while others favor Most patients with myxedema coma have a history of combination of T4 and liothyronine (T3) hypothyroidism. Some patients may have developed an intravenous loading dose of 300-600 micrograms hypothyroidism after thyroidectomy or iodine therapy of levothyroxine (T4) is followed by a daily for hyperthyroidism intravenous doses of 50-100 micrograms Symptoms of hypothyroidism, including fatigue, measurement of thyroid hormones every 1-2 days is weight gain, cold intolerance, constipation, and dry suggested skin, may be elicited. Failure of TSH to decrease or of thyroid hormone Patients have depressed mental states with lethargy, levels to increase suggests the need to increase delirium or coma. Cold Extremities. non-pitting edema doses of T4 and/or add T3 of the upper and lower extremities. Confusion, stupor, the treatment is changed to the oral form once the slow speech, delayed reflexes, seizures, coma patient is able to take medications by mouth ○ symptoms of the precipitating illness can be seen such as infection (commonly pneumonia), stroke, myocardial infarction, D7 GLUCOCORTICOID THERAPY trauma, or heart failure patients with primary hypothyroidism may have concomitant primary adrenal insufficiency while D4 DRASTIC DECREASE IN METABOLIC patients with secondary hypothyroidism may have RATE associated hypopituitarism and secondary adrenal insufficiency hypoventilation leading to respiratory acidosis The other rationale for the treatment with ○ hypothermia corticosteroids is the potential risk of precipitating ○ hypotension acute adrenal insufficiency caused by the accelerated ○ hypoglycemia metabolism of cortisol that follows T4 therapy ○ hyponatremia hydrocortisone at a dose of 50 - 100 mg every 8 ○ hypercapnia hours is administered. an alternative is ○ hypoxia dexamethasone at a dose of 2-4 mg every 12 hours D5 LABORATORY FINDINGS TFTs – TSH (0.4-4 mU/L) is elevated, fT3 and fT4 is D8 SUPPORTIVE MEASURES low. treat hypothermia with passive rewarming using A low or normal TSH levels with low levels of free T4 ordinary blankets and a warm room (0.7-1.9 ng/dK) and free T3 (80-180 ng/dL) may treat associated infection indicate that the disorder is due to pituitary or correct severe hyponatremia with saline and free hypothalamic dysfunction water restriction other test - serum osmolality (hyponatremia), serum correct hypoglycemia and IV dextrose creatinine (because of decreased renal perfusion), Hypotension is usually corrected with thyroid hormone CBC (infection), serum cortisol therapy. If BP continues to be low, cautious use of IV fluids with normal saline is advises D6 MANAGEMENT refractory hypotension can be cautiously treated with vasopressors such as dopamine Levothyroxine sodium - lifelong therapy maintain a patent airway oxygen administration D9 ACTION ALERT IV fluids Myxedema coma can lead to shock, organ damage, vital signs monitoring and death. correct hypothermia vasopressor for tissue perfusion PAGE 15 BERNALES, CORONEL, TURIANO – SY 2024-25 RR42 ACUTE BIOLOGIC CRISIS NCMP119 1ST SEMESTER (PRELIMS) – NACARIO, RN – TUES 7:30-9:30 AM Assess the patient with hypothyroidism, at least every ○ Monitor blood glucose levels, as 8 hrs for changes that indicate increasing severity, severe hypothyroidism can affect especially changes in mental status and report these glucose metabolism promptly to the healthcare provider. ○ collaborate with dietician for treatment is instituted quickly according to the individualized nutritional planning patient’s manifestations and without waiting for laboratory confirmation 4. Impaired Skin Integrity Assessment ○ Assess skin regularly for skin D10 NURSING DIAGNOSIS breakdown, edema, and 1. Decreased Cardiac Output myxedematous changes Assessment ○ monitor pressure points for signs of ○ Monitor vital signs, especially blood pressure ulcer pressure, heart rate, and rhythm. Interventions ○ Assess for signs of poor perfusion ○ implement a turning schedule to (e.g. cyanosis, cold extremities, reposition the patient every 2 hours weak pulses) ○ use pressure relieving devices (e.g. Interventions special mattresses, cushions) ○ administer thyroid hormone ○ keep skin clean and dry replacement therapy as prescribed ○ apply emollients to prevent dryness ○ monitor ECG for bradycardia and and cracking other arrhythmias ○ aminiter IV fluid cautiously to 5. Hypothermia maintain adequate BP Assessment ○ position the pt in a semi-fowlers ○ monitor body temperatur