A practical guide to the management of medical emergencies - part 8 ppt

CHAPTER 72 459 Acute adrenal insuffi ciency Pituitary/hypothalamic disorders: • Postpartum pituitary necrosis (Sheehan syndrome) • Necrosis or bleeding into a pituitary macroadenoma • Head trauma (often associated with diabetes insipidus) • Sepsis or surgical stress in patients with hypopituitarism TABLE 72.3 Urgent investigation in suspected acute adrenal insuffi ciency • Blood glucose • Sodium, potassium and creatinine • Plasma cortisol and corticotropin (10 ml blood in a heparinized tube, for later analysis)* • Full blood count • Coagulation screen • Erythrocyte sedimentation rate and C-reactive protein • Blood culture • Urine stick test, microscopy and culture • Chest X-ray • ECG Typical biochemical fi ndings in acute adrenal insuffi ciency: • Raised creatinine • Low sodium (120–130 mmol/L) • Raised potassium (5–7 mmol/L) • Low glucose • Eosinophilia, lymphocytosis * A plasma cortisol level of >700 nmol/L in a critically ill patient effectively excludes adrenal insuffi ciency. Corticotropin is high in primary and low in secondary adrenal insuffi ciency. 460 SPECIFIC PROBLEMS: ENDOCRINE/METABOLIC Acute adrenal insuffi ciency TABLE 72.4 Management of suspected acute adrenal insuffi ciency Action Comment Investigation Take blood for measurement of cortisol and corticotropin levels (for later analysis), and other investigations (Table 72.3) Exclude/treat Check blood glucose: if <3.5 mmol/L, give 50 ml of hypoglycemia 50% glucose IV via a large vein Fluid replacement 1 L of normal saline over 30 min then 1 L of normal saline over 60 min If systolic BP remains <90 mmHg after 2 L saline, put in a central line and infuse saline to keep the central venous pressure 5–10 cmH 2 O If systolic BP is >90 mmHg, give normal saline 1 L every 6–8 h IV until the fl uid defi cit has been corrected, as judged by clinical improvement and the absence of postural hypotension Hyperkalemia is common in acute adrenal insuffi ciency and potassium should not be added if plasma potassium is >5 mmol/L Steroid Give hydrocortisone 100 mg IV, followed by a replacement continuous infusion of 10 mg/h over the fi rst 24 h Continue hydrocortisone 100 mg IV daily until vomiting has stopped Maintenance therapy is with hydrocortisone 30 mg PO daily which is given in divided doses (20 mg in the morning and 10 mg in the evening) and fl udrocortisone 50–300 µg PO daily Exclude/treat Start antibiotic therapy for suspected sepsis (p. 59) sepsis if a source of sepsis is evident; or if the white cell count is <3 or >20 × 10 9 /L; or if the temperature is <36 or >38°C Confi rm the To confi rm the diagnosis in equivocal cases (where diagnosis and the initial plasma cortisol level is borderline), use underlying cause the short tetracosactrin (Synacthen) test (Table 72.5) CHAPTER 72 461 Acute adrenal insuffi ciency Further reading Arlt W, Allolio B. Adrenal insuffi ciency. Lancet 2003; 361: 1881–93. Cooper MS, Stewart PM. Corticosteroid insuffi ciency in acutely ill patients. N Engl J Med 2003; 348: 727–34. Dorin RI, et al. Diagnosis of adrenal insuffi ciency. Ann Intern Med 2003; 139: 194–204. Vella A, et al. Adrenal hemorrhage: a 25-year experience at the Mayo Clinic. Mayo Clin Proc 2001; 76: 161–8. TABLE 72.5 Short tetracosactrin (Synacthen) test • The test should be done when the patient has recovered from acute illness, as hydrocortisone (but not fl udrocortisone) must be stopped for 24 h before the test. The patient should be resting quietly but need not fast prior to the test • Give 250 µg of tetracosactrin IV or IM before 10 a.m. Measure plasma cortisol immediately before, and 30 and 60 min after the injection • With normal adrenal function, the baseline plasma cortisol is over 140 nmol/L, and the 30 or 60 min level is over 500 nmol/L and at least 200 nmol/L above the baseline level • In patients with primary hypoadrenalism, tetracosactrin does not stimulate cortisol secretion, because the adrenal cortex is already maximally stimulated by endogenous corticotropin. In severe secondary hypoadrenalism, plasma cortisol does not increase because of adrenocortical atrophy. However, in secondary hypoadrenalism which is mild or of recent onset, the test may be normal Thyroid emergencies 73 Thyroid emergencies 462 TABLE 73.1 Thyrotoxic crisis: recognition Clinical features • Fever, abnormal mental state, sinus tachycardia or atrial fi brillation • Signs of thyrotoxicosis, which may not be prominent in the elderly, or may be masked by other illness: check for goitre, thyroid bruit and ophthalmopathy Precipitants • Sepsis • Surgical stress • Trauma • Iodine: amiodarone; radiographic contrast media; radioiodine • Pulmonary embolism, myocardial infarction Urgent investigation • Thyroid hormones (free T3 and free T4*) and TSH (for later analysis) • Blood glucose • Creatinine, sodium and potassium, liver function tests • Full blood count • C-reactive protein • Blood culture • Urine stick test, microscopy and culture • Chest X-ray • ECG • Arterial blood gases and pH T3, tri-iodothyronine; T4, thyroxine; TSH, thyroid-stimulating hormone. * If severely ill, increased production of reverse T3 may lead to near normal thyroxine levels. CHAPTER 73 463 Thyroid emergencies ALERT The mortality of untreated thyrotoxic crisis is high. If the diagnosis is suspected, antithyroid treatment must be started before biochemical confi rmation. TABLE 73.2 Thyrotoxic crisis: management Start antithyroid treatment • Start either propylthiouracil 15–30 mg 6-hourly by mouth or nasogastric tube, reducing to 10–20 mg 8-hourly or after 24 h, or carbimazole (which acts principally by inhibiting thyroxine synthesis) 150–300 mg 6-hourly by mouth or nasogastric tube, reducing to 100–200 mg 8-hourly plus after 24 h • After 4 h, start iodine (which inhibits secretion of thyroxine). If iodine is started before antithyroid drugs, excess thyroxine may be produced leading to an exacerbation of the crisis. Give 0.1–0.3 ml of aqueous iodine oral solution (Lugol solution) 8-hourly by mouth or nasogastric tube. Stop after 2 days if propylthiouracil is used or after 1 week with carbimazole • Give dexamethasone 2 mg 6-hourly PO to inhibit hormone release from the thyroid and reduce the peripheral conversion of thyroxine to tri-iodothyronine • Exchange transfusion or hemodialysis may be considered in a patient who fails to improve within 24–48 h. Seek advice from an endocrinologist Treat heart failure • This is usually associated with fast atrial fi brillation. Cardioversion of atrial fi brillation is very unlikely to be successful until the patient is euthyroid: give digoxin to control the ventricular rate • There is relative digoxin resistance (increased renal excretion and reduced action on AV conduction) so high doses are needed. Loading dose: 0.5 mg IV over 30 min followed by 0.25 mg IV over 30 min every 2 h until the heart rate is <100/min or up to a total dose of 1.5 mg. Maintenance dose: 0.25–0.5 mg daily PO • Give loop diuretic IV as required Continued 464 SPECIFIC PROBLEMS: ENDOCRINE/METABOLIC Thyroid emergencies Start beta-blockade • If there is no pulmonary edema, give propranolol 40–160 mg 6-hourly PO, aiming to reduce the heart rate to <100/min • Diltiazem 60–120 mg 6-hourly PO can be used if beta-blockade is contraindicated because of asthma Start anticoagulation • Give heparin by IV infusion or LMW heparin SC to patients with atrial fi brillation or if pulmonary embolism is suspected (p. 231) • Other patients should receive LMW heparin SC as prophylaxis against venous thromboembolism. Other supportive care • Treat severe agitation with chlorpromazine (50 mg 8-hourly PO; or 25 mg 8-hourly IM; or by rectal suppository 100 mg 6–8 hourly) • Exclude/treat sepsis. • Reduce fever by fanning, tepid sponging or paracetamol (avoid aspirin as it displaces thyroxine from thyroid-binding globulin) • Give fl uid replacement guided by measurement of central venous pressure AV, atrioventricular; LMW, low molecular weight. TABLE 73.3 Myxedema coma: recognition and management Element Comments Clinical features Features suggesting myxedema in the patient with hypothermia: • Preceding symptoms of hypothyroidism: weight gain with reduced appetite, dry skin and hair loss • Previous radio-iodine treatment for thyroxicosis • Thyroidectomy scar • Hyponatremia (plasma sodium <130 mmol/L) • Macrocytosis • Failure of core temperature to rise >0.5°C per hour with external rewarming (Slowly relaxing tendon refl exes are a non-specifi c feature of hypothermia) Continued CHAPTER 73 465 Thyroid emergencies Further reading Cooper DS. Hyperthyroidism. Lancet 2003; 362: 459–68. Roberts CGP, Ladenson PW. Hypothyroidism. Lancet 2004; 363: 793–803. Young R, Worthley LIG. Diagnosis and management of thyroid disease and the critically ill patient. Crit Care Resusc 2004; 6: 295–305. Investigation Thyroid hormones (free T3 and free T4) and TSH (for later analysis) Cortisol (for later analysis) Blood glucose Creatinine, sodium and potassium, liver function tests Full blood count C-reactive protein Blood culture Urine stick test, microscopy and culture Chest X-ray ECG Arterial blood gases and pH Thyroid and Start thyroid hormone replacement with T3 or T4 corticosteroid Give hydrocortisone 100 mg 12-hourly IV in case there hormone is panhypopituitarism replacement T3 has a shorter half-life than T4 which is an advantage if hemodynamic problems develop and the dose has to be reduced • Day 1–3: T3 10 µg 8-hourly IV • Day 4–6: T3 20 µg 12-hourly IV • Day 7–14: T3 20 µg 8-hourly IV An alternative regimen is T4 400–500 µg as a bolus IV or via a nasogastric tube. No further replacement therapy should be given for 1 week Supportive care See management of hypothermia, p. 566 T3, tri-iodothyronine; T4, thyroxine; TSH, thyroid-stimulating hormone. Dermatology/rheumatology Cellulitis 74 Cellulitis 469 Suspected cellulitis Painful swelling and erythema of the skin, typically of the lower leg Key observations (Table 1.2) Focused assessment (Table 74.1); consider differential diagnosis (Table 74.2) Ill patient with severe pain and marked local tenderness? Yes Manage as necrotizing fasciitis Fluid resuscitation (Table 10.2) IV antibiotic therapy (Table 74.3) Seek urgent advice from plastic surgeon and microbiologist No Yes No Yes No Clinical picture typical of cellulitis? IV antibiotic therapy (Table 74.3) Supportive care Improvement after 24–48 h? Change to oral antibiotics Consider other diagnoses (Table 74.2) Refer to dermatologist 470 SPECIFIC PROBLEMS: DERMATOLOGY/RHEUMATOLOGY Cellulitis TABLE 74.1 Urgent investigation in suspected cellulitis • Full blood count • C-reactive protein • Creatinine and electrolytes • Blood culture • Microscopy and culture of blister fl uid if present • Duplex scan if deep venous thrombosis is possible (p. 224) TABLE 74.2 Disorders which may be mistaken for cellulitis Disorder Distinguishing features Necrotizing fasciitis Ill patient Severe pain, disproportionate to physical signs Skin may be very tender, with blue-black discoloration and blistering Rapid clinical progression Leg eczema (venous Longer history eczema or contact May be bilateral (bilateral cellulitis is rare) dermatitis) No fever or systemic symptoms (NB cellulitis may Itching rather than tenderness of the skin complicate eczema) History of varicose veins or DVT Crusting or scaling (in cellulitis the skin is typically smooth and shiny) Deep vein Proximal margin of erythema usually not well thrombosis (DVT) demarcated (NB cellulitis may If clinical setting suggests DVT (p. 224), duplex complicate DVT) scan of leg veins needed to exclude this Allergic reaction to No ascending lymphangitis insect sting or bite Itching Continued [...]... polyarteritis Antinuclear antibody Anti-double-stranded DNA antibody Rarely, p-ANCA Low complement Usually present Usually present Usually present Uncommon Usually present Uncommon Systemic lupus erythematosus ANCA, antineutrophil cytoplasmic antibodies; c-ANCA, antibodies with a cytoplasmic pattern of staining; p-ANCA, antibodies with a perinuclear pattern of staining; ESR, erythrocyte sedimentation... hemorrhage Asthma Neuropathy Palpable purpura Gastrointestinal bleeding Abdominal pain Hematuria Palpable purpura Arthralgia Drug history Palpable purpura Maculopapular rash Microscopic polyarteritis Churg–Strauss arteritis Henoch–Schönlein purpura Drug-induced vasculitis Microscopic hematuria or red cell casts Biopsy of involved tissue shows granulomatous arteritis or periarteritis Transient shadowing... disease Causes/comment See Tables 63.1, 87 .1 and 87 .2 Hypothyroidism may also cause normocytic anemia See p 394 Other blood results Abnormal liver function tests, with raised AST (>ALT) and gamma GT Raised TSH, low free T4/free T3 Abnormal liver function tests/prothrombin time Interpretation of full blood count ALT, alanine aminotransferase; AST, aspartate aminotransferase; gamma GT, gamma glutamyl transferase;... Microcytic anemia (MCV < 78 fl) Normal ferritin Hemoglobin electrophoresis normal in alphathalassemia trait and abnormal in betathalassemia trait and other thalassemia syndromes Low iron Low/normal transferrin Normal/increased ferritin Low iron Increased transferrin Low ferritin Other blood results Interpretation of full blood count Continued Hematocrit usually >30% and MCV . meropenem TABLE 75.5 Management of acute arthritis Cause of acute arthritis Management Septic arthritis Antibiotic therapy (Table 75.4) Joint drainage Seek advice from orthopedic surgeon/rheumatologist Continued CHAPTER. Septic arthritis Infl ammatory erythematosus Trauma* bowel disease Viral diseases (e.g. Hemarthrosis Reactive arthritis rubella, hepatitis secondary to following gut B and C, warfarin or genitourinary. similar attacks of arthritis? • History of trauma? • Possible septic arthritis? Septic arthritis usually follows a bacteremia (e.g. from IV drug use) in a patient at risk because of rheumatoid arthritis,