 \212 \212Acidosis can be present without gross elevation of glucose; when this occurs, consider other causes as well (e.g., salicylates, lactic acidosis). Serum amylase mon, even in the absence of pancreatitis. \212 is often elevated, and nonspecific abdominal pain is com- Management See Table 20.21. Dehydration is more life-threatening than hyperglycemia, so its correction takes precedence. See Table 20.22. \212 Monitor electrolytes carefully, especially potassium levels (which may fall during therapy) , glucose, creatinine, HCO 3, hourly initially. Aim for a fall in glucose of 90 mg/dL/h a nd correction of the acidosis. The use of venous HCO 3 can be used as a guide to progress and may prevent the need for repeated ABG sampling. K + disturbance may cause dysrhythmias . See Table 20.23. Flow chart vital signs, fluids inputs and output (urine output), and ket ones; insert Foley catheter if no urine is passed for >4 h. Monitoring CVP OR ultrasound IV C measurement may sometimes be helpful in guiding fluid replacement. Find and treat infecti on (lung, skin, perineum, urine after cultures). \212 \212 NB: If acidosis is severe (pH <7), some give IV bicarbonate. This remains controversi al because of effects on the HG-dissociation curve and cerebral circulation \200\224discuss with your senior resident. Complications Cerebral edema, aspiration pneumonia, hypokalemia , hypomagnesemia, hypophosphatemia, thromboembolism. Talk with the patient: Ensure that the re are no further preventable episodes or other complicating issues. Other emergencies: Hyp erosmolar nonketotic coma and hypoglycemia 780 e n i c i d e m y c n e g r e m E Table 20.21 DKA Management plan IV access and start fluid (0.9% saline or lactated Ringer \200\231s) replacement immediatel y \206\223 Check plasma glucose: Usually >200 mg/dL if so give 4 \200\2238 U (0.1 U/kg) re gular insulin IV \206\223 Investigate precipitating cause \206\223 Labs electrolytes, glu cose, CMP , osmolality, blood gasses, CBC, serum ketones, blood culture, mg, phos, Ca, CXR, ECG Urine tests: Ketones, urine C+S \206\223 Insulin sliding scale (below) \206\223 Cont inue fluid replacement, K + replacement \206\223 Check glucose and CMP regularly (hourly i nitially) \206\223 Continue the investigation of causes Table 20.22 Fluid replacement \212 Give 1 L of 0.9% saline immediately. Then, typically, 1 L over the next hour, 1 L over 2 h, 1 L over 4 h, then 1 L over 6 h. Use dextrose saline or 5% dextrose when blood glucose is <259 \200\223300 mg/dL. Those >65 yrs or with CHF need less saline and more cautious fluid delivery. \212 \212 Table 20.23 Potassium replacement \212 Total body potassium is invariably low, and plasma K cells with treatment. Don \200\231t ad d K + to the first bag. Less will be required in renal failure or oliguria. Determine Urine output prior to K replacement. Check CMP every 2 h initially and replace K + as needed. + falls as K + enters \212 781 Other diabetic emergencies Hypoglycemic coma Usually rapid onset; may be preceded by odd be havior (e.g., aggression), sweating, pulse \206\221 , seizures. Management: Give 20 \200 \22330 g dextrose IV (e.g., 200 \200\223300 mL of 10% dextrose). This is preferable to 50 \200\223100 mL 50% dextrose, which may harms veins. Expect prompt recovery. Glucagon 1 mg I V/IM is nearly as rapid as dextrose but will not work in intoxicated patients. Dextrose IV may be needed for severe prolonged hypoglycemia. Once conscious, give sugary drinks and a m eal. Hyperglycemic hyperosmolar nonketotic state Those with type 2 diabetes are at risk of this. The history is longer (e.g., 1 wk), with marked dehydration and glucose >800 mg/dL. A cidosis is absent as there has been no switch to ketone metabolism \200\224the patient is o ften older and presenting for the first time. The osmolality is >340 mosmol/kg. Focal CNS s igns may occur. The risk of DVT is high, so consider anticoagulation. Rehydrate over 48 h w ith 0.9% saline IV (e.g., at half the rate used in ketoac- idosis). Wait an hour before giv ing any insulin (it may not be needed, and you want to avoid rapid changes). If it is neede d, 1 U/h is a typical initial dose. Look for the cause (e.g., MI, or bowel infarct). Hyperl actatemia is a rare but serious complication of DM(e.g., after septicemia or biguanide use) . Blood lactate: >5 mmol/L. Seek expert help. Give O 2 . Treat any sepsis vigorously. Thyroid emergencies Myxedema coma Signs and symptoms: Patient looks hypothyroid; >65 yrs, h ypothermia, hyporeflexia, glucose \206\223 , bradycardia, coma, seizures. History: Prior s urgery or radioiodine for hyperthyroidism. Precipitants: Infection, MI, stroke, trauma. Exa mination: Goiter, cyanosis, heart failure, precipitants. Treatment: Preferably in intensive care. \212 Take venous blood for T3, T4, thyroid-stimulating hormone (TSH), CBC, CMP, cultures, cortis ol. Take arterial blood for Give high-flow O 2 if cyanosed. Correct any hypoglycemia. Give T3 (triiodothyronine) 5 \200\22320 mcg IV slowly. Be cautious: This may precipitate manifes tations of undiagnosed ischemic heart disease. Give hydrocortisone 100 mg/8 h IV \200\224vi tal if pituitary hypothyroidism is suspected (i.e., no goiter, no previous radioiodine, no thyroid surgery). IV 0.9% saline. Be sure to avoid precipitating LVF. If infection suspecte d, give antibiotic (e.g., cefuroxime 1.5 g/8 h IVI). Treat Treat tions (hypoglycemia, pancr eatitis, arrhythmias). \212 \212 \212 P a O 2 . \212 \212 \212 \212 \212 heart failure as appropriate. hypothermia with warm blankets in warm room. Beware complica- Further therapy: T3 5 \200\22320 mcg/4 \200\22312 h IV until sustained improvement (e.g., 2 \200\2233 d), then thyroxine (T4 = levothyroxine) 50 mcg/24 h PO. Continue hydrocortisone . Give IV fluids as appropriate (hyponatremia is dilutional). Hyperthyroid crisis (thyrotox ic storm) Signs and symptoms: Severe hyperthyroidism: Fever, agitation, confusion, coma, ta chycardia, AF, vomiting and diarrhea, goiter, thyroid bruit, \200\234acute abdomen \200 \235 picture. Precipitants: Recent thyroid surgery or radioiodine, infection, MI, trauma. D iagnosis: Confirm with technetium uptake if possible, but do not wait for this if urgent tr eatment is needed. Treatment: Enlist expert help from an endocrinologist. See Table 20.24. 782 e n i c i d e m y c n e g r e m E Table 20.24 Management plan for thyrotoxic storm IV 0.9% saline, 500 mL/4 h; NG tube if vomiting. \206\223 Take blood for: T3, T4, cultures (if infection suspected) \206\223 Sedate if necessary (e.g., midazolam 2 mg IV) \206\223 If no contraindication, give propranolol 40 mg/8 h PO (maximum IV dose: 1 mg over 1 min, r epeated up to 9 times at \211 2 min intervals) \206\223 High-dose digoxin may be needed to slow the heart (e.g., 1 mg over 2 h IV) \206\223 Antithyroid drugs: Propylthiouracil (P TU 50 \200\223200 mg q4h) \206\223 Hydrocortisone 100 mg/6 h IV or dexamethasone 4 mg/6 h PO \206\223 Treat suspected infection with, e.g., cefuroxime 1.5 g/8 h IV \206\223 Adjust IV fluids as necessary; cool with sponging acetaminophen Addisonian crisis Signs and symptoms: May present in shock (tachycardia, peripheral vaso- c onstriction, postural hypotension, oliguria, weak, confused, comatose). Typically (but not always!) seen in a patient with known Addison \200\231s disease or in someone on long-term steroids who has forgotten to take tablets. An alternative presentation is with hypoglycemi a. Precipitating factors: Infection, trauma, surgery. Management: If suspected, treat befor e biochemical results. \212 Take blood for cortisol (10 mL heparin or clotted) and adrenocortico- tropic hormone (ACTH) if possible (10 mL heparin, to go straight to laboratory). Hydrocortisone sodium succinate 100 mg IV stat. IV: Use 0.9% saline or lactated Ringer \200\231s solution for resuscitatio n. Monitor blood glucose: The danger is hypoglycemia. Take blood, urine, sputum for culture . Give antibiotics (e.g., cefuroxime 1.5 g/8 h IV). \212 \212 \212 \212 \212 Continuing treatment: \212 \212 \212 \212 Glucose IV may be needed if hypoglycemic. Continue IV fluids, more slowly. Be guided by cli nical state. Continue hydrocortisone sodium succinate 100 mg IV/IM q6h. Change to oral ster oids after 72 h if patient \200\231s condition is good. The ACTH stimulation test (cosyntro pin) is impossible while on hydrocortisone. Fludrocortisone is needed only if hydrocortison e dose is <50 mg/d and the condition is due to adrenal disease. Search for the cause once t he crisis is over. 783 \212 \212 Hypopituitary coma Usually develops gradually in a person with known hypopituitarism. Rarel y, the onset is rapid due to infarction of a pituitary tumor (pituitary apoplexy); because symptoms include headache and meningismus, subarachnoid hem- orrhage is often misdiagnosed. Presentation: Headache, ophthalmoplegia, consciousness \206\223 , hypotension, hy- pother mia, hypoglycemia, signs of hypopituitarism. Tests: T4, cortisol, TSH, ACTH, glucose; pitui tary fossa CT/MRI. Treatment: \212 \212 \212 Hydrocortisone sodium succinate 100 mg IV/6 h Only after hydrocortisone begun: T3 10 mcg/12 h PO Prompt surgery is needed if the cause is pituitary apoplexy. Pheochromocytoma emergencies Stress, abdominal palpation, parturition, general anesthetic, or contrast media used in radiography may produce dangerous hypertensive crises (pal- lor, pulsating headache, hypertension, feels \200\234about to die \200\235). Treatment Get help . \212 \212 \212 Phentolamine 2 \200\2235 mg IV; repeat to maintain safe BP. Labetalol is an alternative age nt. When BP is controlled, give phenoxybenzamine 10 mg/24 h PO( \206\221 by 10 mg/d as nee ded, up to 0.5 \200\2231 mg/kg/12 h PO); SE : Postural hypotension, dizziness, tachycardia, nasal congestion, miosis, idiosyncratic marked BP drop soon after exposure. The idea is to increase the dose until the BP is controlled and there is no significant postural hypotens ion. A \222 -blocker may also be given at this stage. Surgery is usually done electively a fter a period of 4 \200\2236 wks, to allow full -blockade and volume expansion. When adm itted for surgery, the phenoxy- benzamine dose is increased until significant postural hypo tension occurs. \212 Acute renal failure (ARF) Seek expert help promptly: BP, urinary sediment, serum K + , crea tinine, and US must be rapidly known. Have them at hand. Definition Acute (over hours or da ys) deterioration in renal function, characterized by a rise in serum creatinine and urea, often with oliguria or anuria. Causes \212 \212 \212 \212 \212 \212 Investigations \212 Hypovolemia Low cardiac output Sepsis Drugs Obstruction Other (e.g., hepatorenal syndrome, vasculitis) 2+ , PO3 CMP, Ca 4 , CBC, ESR, CRP, INR, LFT, CK, lactose dehydrogenase (LDH), protein electrophores is, hepatitis serology, autoantibodies, blood cultures. Urgent urine microscopy and culture s. White cell casts suggest infection, but are seen in interstitial nephritis, and red cell casts are seen in inflam- matory glomerular conditions. US of the renal tract ECG, CXR \212 784 \212 \212 See Table 20.25 for acute measures. Underlying Management principles are: Treat precipitating cause: Treat acute blood loss with blood tra nsfusion, and treat sepsis with antibiotics. ARF is often associated with other diseases th at need more urgent treatment. For example, someone in respiratory failure and renal failur e may need to be managed in the ICU, not in a renal unit, to ensure optimal management of t he respiratory failure. Treat life-threatening hyperkalemia: See Table 20.26. Treat pulmona ry edema, pericarditis, and tamponade: Urgent dialysis may be needed. If in pulmonary edema and no diuresis, consider removing a unit of blood before dialysis commences. Treat volume depletion if necessary: Resuscitate quickly; then match input to output. Use a large-bore line in a large vein (central vein access can be risky in obvious volume depletion). Treat sepsis Further care \212 e n i c i d e m y c n e g r e m E Has obstruction been excluded? Examine for rectal and vaginal masses; arrange urgent US. Is the bladder palpable? Bilateral nephrostomies relieve obstruction, provide urine for cultu re, and allow pyelography to deter- mine the site of obstruction. If worsening renal functi on but dialysis-independent, consider renal biopsy. Diet: tein. Consider nasogastric feedin g or parenteral route if too ill. \212 \212 High in calories (2,000 \200\2234,000 kcal/d) with adequate high-quality pro- Prognosis Depends on cause ( ATN mortality : Surgery or trauma, 60%; medical illness, 30%; pregnancy, 10%). Oliguric ARF is worse than nonoliguric with more GI bleeds, sepsis, acidos is, and higher mortality. Urgent dialysis if: K \212 + persistently high (>6.0 meq/L) \212 \212 \212 Acidosis (pH <7.2) Pulmonary edema and no substantial diuresis Pericarditis (In tamponade, only dialyze relieved.) High catabolic state with rapidly progressive renal failure after pressure on the heart is \212 785 Table 20.25 Management of ARF Catheterize to assess hourly urine output, and establish fluid charts \206\223 Assess intr avascular volume BP, JVP, skin turgor, fluid balance sheet, weight, CVP, attach to cardiac monitor. Consider inserting a central venous cannula \206\223 Investigations \206\223 Ide ntify and treat hyperkalemia \200\224see below Use a cardiac monitor \206\223 If dehydrate d Fluid challenge: 250 \200\223500 mL of colloid or saline over 30 min \206\223 Reassess R epeat if still fluid depleted. Aim for a CVP of 5 \200\22310 cm H 2 O \206\223 Once fluid replete, continue fluids at 20 mL + previous hour \200\231s urine output per hour \206\223 If volume overloaded, consider urgent dialysis A nitrate infusion, or furosemide may help in the short term, especially to make space for blood transfusion etc. but does not alter o utcome \206\223 If clinical suspicion of sepsis, take cultures, then treat vigorously Do n ot leave possible sources of sepsis (e.g., iv lines) in situ unless unavoidable \206\223 A void nephrotoxic drugs (e.g., NSAIDs, ACE-inhibitors, gentamicin) Check Medication Sheet fo r all drugs given. Table 20.26 Hyperkalemia The danger is ventricular fibrillation. A K + of >6.5 mEq/L will usually require urgent tre atment, as will those with ECG changes: \212 \212 Tall \200\234tented \200\235 T-waves flat P-waves Widening of the QRS complex leads eventually, and dangerously, to a sinusoidal pattern and VF/VT. \206\221 PR interval. Treatment: \212 10 mL calcium gluconate (10%)IV over 2 min, repeated as necessary if severe ECG changes. Th is provides cardioprotection. It does not change serum potassium levels. Insulin + glucose (e.g., 10 units regular insulin + 50 mL of glucose 50% IV). Insulin moves K + into cells. N ebulized albuterol (2.5 mg) also makes K Polystyrene sulfonate resin (e.g., Kayexalate, 15 g/8h in water) orally or, if vomiting makes the PO route problematic, as a 30 g enema (foll owed by colonic irrigation after 9 h, to remove K + from the colon). Dialysis \212 \212 \212 + enter cells. 786 \212 Acute poisoning: General measures Diagnosis comes mainly from history. The patient may be r eluctant or unwilling to tell the truth about what has been taken. Pill identification is o ccasionally helpful, and texts such as the Physician \200\231s Desk Reference (PDR) may use ful. Multiple ingestions are common. While awaiting the results of the serum and urine toxi cological screen, certain physical findings may help to narrow the potential drugs ingested . \212 e n i c i d e m y c n e g r e m E Albuterol, antimuscarinics, tricyclics, quinine, or Fast or irregular pulse: phenothiazine poisoning Respiratory depression: Hypothermia: \212 \212 \212Hyperthermia: Amphetamines, monoamine oxidase inhibitors (MAOIs), Opiate or benzodiazepine toxicity Phenothiazines, barbiturates cocaine, or ecstasy Coma: Seizures: ines, or theophyllines Constricted pupils: Dilated pupi ls: Hyperglycemia: Hypoglycemia: Renal failure: Metabolic acidosis: carbon monoxide poisoni ng \212 \212 Benzodiazepines, alcohol, opiates, tricyclics, or barbiturates Recreational drugs, hypoglycemic agents, tricyclics, phenothiaz- \212 \212 \212 \212 \212 \212 Opiates or insecticides Amphetamines, cocaine, quinine, or tricyclics Organophosphates, theophyllines, or MAOIs Ins ulin, oral hypoglycemics, alcohol, or salicylates Salicylate, acetaminophen, or ethylene glycol Alcohol, ethylene glycol, methanol, acetaminophen, or \212 \206\221 Osmolality: Alcohols (ethyl or methyl), ethylene glycol Management See Table 20.27 for a general guide to management. \212 as appropriate. Always check acetaminophen and salicylate Take blood levels. Empty stomach Consider specific antidote If you are not familiar with th e poison, Poison Control Center. \212 \212 \212 if appropriate. or oral activated charcoal. get more information. Call your local Continuing care Measure temperature, pulse, BP, and blood glucose regularly. Use a continuo us ECG monitor. If unconscious, turn regularly, keep eyelids closed. A urinary catheter wil l be needed if the bladder is distended, renal failure is suspected, or forced diuresis is undertaken. Take to ICU, e.g., if respiration decreases. Psychiatric assessment Be sympathe tic despite the hour! Interview relatives and friends if possible. Aim to establish: \212 Was the act planned? What precautions against being Intentions at time: found? Did the pati ent seek help afterward? Does the patient think the method was dangerous? Was there a final act (e.g., suicide note)? Present intentions What problems Was the act Is there a schizoph renia, dementia)? What are his \212 \212 \212 \212 led to the act: Do they still exist? aimed at someone? psychiatric disorder (depression, alcoholism, personality disorder, \212 resources (friends, family, work, personality)? The assessment of suicide risk: The f ollowing increase the chance of future suicide: Original intention was to die, present inte ntion is to die, presence of psychiatric disorder, poor resources, previous suicide attempt s, socially isolated, unemployed, male, >50 yrs old. Referral to psychiatrist: This depends partly on local resources. Ask advice if presence of psychiatric disorder or high suicide risk. 787 Table 20.27 Emergency care for poisoining ABC \200\231s, clear airway \206\223 Consider ventilation (if the respiratory rate is <8/m in, or P a O 2 <60 mm Hg, when breathing 60% O 2 , or the airway is at risk, e.g., GCS <8) \206\223 Treat shock Further management \206\223 Assess the patient \206\223 History from patient, friends, or family is vital \206\223 Features from the examination may help \206\223 Investigations Glucose, CMP, CBC, LFT, INR, ABG, ECG, lactate, acetaminophen, and salicylate levels, urine /serum toxicology, specific assays as appropriate \206\223 Monitor T (rectal) , pulse, an d respiratory rate, BP, O 2 saturations, urine output ECG \206\223 Treatment Supportive measures: May need catheterization \206\223 Absorption: Consider gastric lavage activa ted charcoal Consider naloxone if unconscious and pin-point pupils Acute poisoning: Specific points Plasma toxicology For all unconscious patients, acetaminop hen and aspi- rin levels and blood glucose are required. The necessity of other assays depe nds on the drug taken and the index of suspicion. Be guided by the poison information servi ce. More common assays include digoxin, metha- nol, lithium, iron, theophylline. Toxicologi cal screening of urine, especially for recreational drugs, may be of use in some cases. Gas tric lavage In general, only of use if presentation is within 40 min of ingestion and if a potentially toxic dose of a drug has been taken. Lavage beyond this time frame may make mat ters worse. Do not empty the stomach if petroleum products or corrosives such as acids, alk alis, bleach, have been ingested ( exception : Paraquat) or if the patient is unconscious o r unable to protect his airway (unless intubated). Never induce vomiting. Gastric emptying and lavage Gastric emptying and lavage is contraindicated in patients who have a change in mental status, who are comatose, or have an absent gag reflex. These patients may require e ndotracheal intubation prior to insertion of a nasogastric tube. If conscious, get verbal c onsent. 788 \212 \212 \212 \212 \212 Monitor O Have suction apparatus at hand and working. Position the patient in left lateral position. Raise the foot of the bed by 20 cm. Pass a lubricated tube (14 mm external diamet er) via the nares, asking the patient to swallow. Confirm position in stomach: Blow air dow n and auscultate over the stomach. Siphon the gastric contents. Check pH with litmus paper. Perform gastric lavage using 300 \200\223600 mL tepid water at a time. Repeat until no tab lets in siphoned fluid. Leave activated charcoal (50 g in 200 mL water) in the stomach unle ss alcohol, iron, Li + , or ethylene glycol was ingested. When pulling out tube, occlude it s end (prevents aspiration of fluid remaining in the tube). 2 by pulse oximetry. e n i c i d e m y c n e g r e m E \212 \212 \212 \212 \212 \212 Activated charcoal reduces the absorption of many drugs from the gut when given as a single dose of 50 g with water (e.g., salicylates, acetaminophen). It is given in repeated doses (50 g q4h) to increase the elimination of some drugs from the blood (e.g., carbamazepine, d apsone, theophyllines, quinine, digoxin, phenytoin, phenobarbitone (phenobarbital), and par aquat). Lower doses are used in children. Some specific poisons and their antidotes Benzodiazepines Flumazenil rarely used (for respi ratory arrest) 200 mcg over 15 sec; then 100 mcg at 60 sec intervals if needed. Usual dose range: 300 \200\223 600 mcg IV over 3 \200\2236 min (up to 1 mg; 2 mg if on ITU). May provo ke seizures. \222 -Blockers Severe bradycardia or hypotension. Try atropine up to 3 mg IV. Give glucagon 2 \200\22310 mg IV bolus + 5% dextrose if atropine fails ( an atropine inf usion of 50 mcg/kg/h). consider prophylactic antiemetic since glucagon provokes nausea and vomiting. If unresponsive, consider pacing or an aortic balloon pump. Cyanide This fast-kil ling poison has affinity for Fe 3+ and inhibits the cytochrome system, reducing aerobic res piration. Three phases: 1. Anxiety confusion 2. Pulse \206\221 or \206\223 3. Seizures shock coma. Treatment: 100% O 2 , GI decontamination; if reduced consciousness, give ampule of amyl nitrate for inhalation (if no IV established), 10 cc of 3% solution sodium nitrate IV, and 50 cc of 25% solution of sodium thiosulfate. Alternatively consider hydroxo cobalamin 5gm IV over 15 min. Get expert help Carbon monoxide Despite hypoxemia, skin is pi nk (or pale), not blue, as carboxyhemoglobin (COHb) displaces O2 from Hb binding sites. Sym ptoms: Headache, vomiting, pulse \206\221 , tachypnea, and, if COHb >50%, fits, coma, and cardiac arrest. Remove the source. Give 100% O2. Metabolic acidosis usually responds to cor rection of hypoxia. If severe, anticipate ce- rebral edema. Give mannitol IV. Confirm diagn osis with a heparinized blood sample (COHb >10%) quickly as levels may soon return to norma l. Moni- tor ECG. Hyperbaric O 2 may help: Discuss with the poison service if patient is or has been unconscious, pregnant, COHb >20%, or failing to respond. Digoxin Symptoms: Cognit ion \206\223 , yellow-green visual halos, arrhythmias, nausea, and anorexia. If serious ar rhythmias are present, correct hypokalemia and inactivate with digoxin-specific antibody fr agments (Digibind ). If load or level is unknown, give 20 vials (800 mg) for adult or chil d >20 kg. Consult 789 Poison Control. Dilute in water for injections (4 mL/38 mg vial) and 0.9% saline (to make a convenient volume); give IV over half hour, via a 0.22 mcm-pore filter. If the amount of d igoxin ingested is known, Poison Control will tell you how many vials of Digibind to give (e.g., if 25 tabs of 0.25 mg ingested, give 10 vials; if 50 tabs, give 20 vials; if 100 ta bs, give 40 vials). Heavy metals Enlist expert help. Iron Deferoxamine 15 mg/kg/h IV; max 8 0 mg/kg/d. NB: Gastric lavage if iron ingestion in last hour; consider whole bowel irrigati on. Oral anticoagulants If major bleed, treat with vitamin K, 5 mg slow IV; give prothrombi n complex concentrate 50 U/kg IV(or, if unavailable, fresh frozen plasma 15 mL/kg IV). If i t is vital that anticoagulation continues, enlist expert help. Warfarin can normally be res tarted within 2 \200\2233 d. NB: Coagulation defects may be delayed for 2 \200\2233 d follo wing ingestion. Opiates Many analgesics contain opiates. Give naloxone (e.g., 0.8 \200\2232 mg IV); repeat every 2 min until breathing adequate (it has a short t , so it may need to be given often or IM; max 10 mg). Naloxone may precipitate features of opiate withdrawal : Diarrhea and cramps will normally respond to diphenoxylate and atropine (Lomotil ; e.g., 2 tablets/6 h PO). Sedate as needed. Phenothiazine poisoning (e.g., chlorpromazine) No spe cific antidote. Dystonia (torticollis, retrocollis, glossopharyngeal dystonia, opisthotonus ): Try benztropine 1 \200\2232 mg IV/IM. Treat shock by raising the legs ( plasma expande r IV or norepinephrine IV if desperate). Restore body temperature. Monitor ECG . Avoid lido caine in dysrhythmias. Use diazepam IV for prolonged seizures. Neuroleptic malignant syndro me : Hyperthermia, rigidity, extrapyramidal signs, autonomic dysfunction (labile BP, pulse \206\221 , sweating, urinary incontinence), mutism, confusion, coma, WBC \206\221 , CPK \206\221 ; it may be treated with cooling. Dantrolene has been tried. Carbon tetrachloride poisoning This solvent, used in many industrial processes, causes vomiting, abdominal pain, diarrhea, seizures, coma, renal failure, and tender hepatomegaly with jaundice and liver f ailure. IV acetylcysteine may improve prognosis. Seek expert help. Organophosphate insectic ides inactivate cholinesterase; the resulting increase in acetylcholine causes the SLUD res ponse: S alivation, lacrimation, urination, and diarrhea. Also look for sweating, small pup ils, muscle fasciculation, coma, respiratory distress, and bradycardia. Treatment: Wear glo ves; remove soiled clothes. Wash skin. Take blood (CBC and serum cholinesterase activity). Give atropine IV = 2 mg every 10 min until full atropinization (skin dry, pulse >70, pupils dilated). Up to 3 d treatment may be needed. Also give pralidoxime 30 mg/kg slowly. Repeat as needed every 30 min; max 12 g in 24 h. Even if seizures are not occurring, diazepam 5 \200\22310 mg IV seems to help. Paraquat poisoning Found in weed-killers. This causes painf ul oral and esophageal ulcers, alveolitis, and renal failure. Diagnose by urine test. Give activated charcoal at once (100 g followed by a laxative, then 50 g/3 \200\2234 h, antie metic). Get expert help . Avoid O 2 early on (promotes lung damage). Ecstasy poisoning Ecst asy is a semisynthetic hallucinogenic substance (MDMA, 3,4-methylenedioxymethamphetamine). Its effects range from nausea, muscle pain, blurred vision, amnesia, fever, confusion, and ataxia to tachyarrhythmias, hyperthermia, hyper/hypotension, water intoxication, DIC, K + \206\221 , acute renal failure, hepatocellular and muscle necrosis, cardiovascular collapse , and ARDS. There is no antidote, and treatment is supportive. 790 Management depends on clinical and lab \201 ndings, but may include: \212 e n i c i d e m y c n e g r e m E Administration of activated charcoal and monitoring of BP, ECG, and temperature for at leas t 12 h (rapid cooling may be needed). Monitor urine output and CMP, LFT, creatinine kinase, platelets, and coagulation. Metabolic acidosis may benefit from treatment with sodium bica rbonate. Anxiety: Diazepam 0.1 \200\2230.3 mg/kg PO. Max IV does over 2 min Narrow complex tachycardias in adults: Consider metoprolol 5 \200\22310 mg IV. Hypertension can be treated with nifedipine 5 \200\22310 mg PO or phentolamine 2 \200\2235 mg IV. Treat hypotension co nventionally. Hyperthermia: Attempt to cool, if rectal T >39 C. Consider dantrolene 1 mg /kg IV (may need repeating: Discuss with your senior and a poison unit). Hyperthermia with ecstasy is akin to serotonin syndrome, and pro- pranolol, muscle relaxation, and ventilatio n may be needed. \212 \212 \212 \212 \212 Snakes and Snake envenomation : There are two types of poisonous snakes in the United State s, the pit viper (rattlesnake) and the elapid (coral snake) For suspected envenomations, co nsider giving 1 \200\2232 vials of specific antivenom as soon as possible. To locate antise ra for exotic snakes, call a regional poison control center (800 \200\223222 \200\2231222). CroFab is now available for pit viper bites, and 4 \200\2236 vials should be given if ther e is evidence of local or systemic reaction Management: Avoid active movement of affected l imb (use splints/slings). Avoid incisions and tourniquets . Get help. Salicylate poisoning Aspirin is a weak acid with poor water solubility. It is present in ma ny over-the-counter preparations. Anaerobic metabolism and the production of lactate and he at are stimulated by the uncoupling of oxidative phospho- rylation. Effects are dose-relate d and potentially fatal: \212 \212 \212 Signs and symptoms Unlike acetaminophen, many ea rly features. Vomiting, dehydration, hyperventilation, tinnitus, vertigo, sweating. Rarely, lethargy or coma, seizures, vomiting, \206\223 BP and heart block, pulmonary edema, hyper thermia. Patients present initially with respiratory alkalosis due to a direct stimulation of the central respiratory centers and then develop a metabolic acidosis. Hyper- or hypogly cemia may occur. Management Correct dehydration. Gastric lavage if within 1 h, activated ch arcoal (may be repeated, but is of unproven value). \212 150 mg/kg: 250 mg/kg: >500 mg/kg: Mild toxicity Moderate Severe toxicity Acetaminophen and salicylate level, glucose, CMP, LFT, INR, ABG, ,CBC. Salicylate level may need to be repeated after 2 h due to continuing absorption if a potentially toxic dose has been taken. Levels over 700 mg/L are potentially fatal. Monitor urine output and blood glu cose. If severe poisoning: Salicylate levels, blood pH, and CMP. Consider urinary catheter and monitoring urine pH. Beware hypoglycemia. If plasma level >500 mg/L (3.6 mmol/L), consi der alkalinization of the urine, with IV sodium bicarbonate. Aim to make the urine pH 7.5 \200\2238.5. NB: Monitor serum K + because hypokalemia may occur. Consider dialysis if plas ma level >700 mg/L, and if patient has renal or heart failure, seizures, severe acidosis, o r persistently \206\221 plasma salicylate. ECG monitor. Discuss any serious cases with the local toxicological service or national poison information service. \212 \212 \212 \212 791 \212 Acetaminophen poisoning 140 mg/kg (or 12 g) in adults may be fatal. However, prompt treatme nt can prevent liver failure and death. Signs and symptoms None initially, or vomiting R UQ pain. Later: Jaundice and encephalopathy from liver damage (the main danger) renal fa ilure. Management General measures : Lavage if >12 g (or >140 mg/kg) taken within 1 h. Give activated charcoal if <8 h since ingestion. Specific measures: \212 , FBC; blood level at Glucose, CMP, LFT, INR, ABG, PT/PTT/INR, HCO 3 4 h postingestion If <8 h since overdose and plasma acetaminophen is above the line on the graph in Figure 20.3 , start N -acetylcysteine. If >8 h and suspicion of large overdose (>7.5 g) err on the side of caution and start acetylcysteine, stopping it if acetaminophen level is below the treat ment line and INR and ALT are normal. Acetylcysteine is given by IV: 140 mg/kg in 200 mL of 5% dextrose over 15 min. Then 50 mg/kg in 500 mL of 5% dextrose over 4 h. Then 100 mg per kg/16 h in 1 L of 5% dextrose. Rash is a common SE: Treat with diphenhydramine and observe; do not stop unless anaphylaxis (i.e., shock, vomiting, wheeze occurs [<10%]). If ingestion time is unknown, it is staggered, or presentation is >15 h from ingestion, treatment may h elp. Get advice. \206\223 ), if long-acting The graph may mislead if HIV positive(hepatic glutathione acetaminophen has been taken, in the presence of preexisting liver dis- ease, o r if induction of liver enzymes has occurred. Beware glucose \206\223 ; bedside glucose/1h r; INR/12 h. Next day, do PT, PTT, INR, CMP, LFT. If INR rising, continue acetyl- cysteine until <1.4. If continued deterioration, discuss with the liver team. \212 \212 \212 \212 \212 \212 \212 Do not hesitate to get expert advice. Criteria for transfer to ICU: \212Encephalopat hy or ICP \206\221 . Signs of CNS edema: BP >160/90 (sustained) or brief rises (systolic > 200 mm Hg), bradycardia, decerebrate posture, extensor spasms, poor pupil responses. ICP mo nitoring can help. INR>2.0 at <48 h or >3.5 at <72 h (so measure INR q12h). Peak elevation: 72 \200\22396 h. LFTs are not good markers of hepatocyte death. If INR is normal at 48 h, the patient may go home. \212 \212Renal impairment (creatinine >2.2 mg/dL). Monitor urine flow. Daily CMP and serum creatinine (use hemodialysis if >2.4 mg/dL). \212Blood pH <7.3 (lactic acidosis \206\222 tissue hypoxia) \212Systolic BP <80 mm Hg 792 e n i c i d e m y c n e g r e m E Figure 20.3 Patients whose plasma-acetaminophen concentrations are above the nor- mal treatment line sh ould be treated with acetylcysteine by IV infusion (or, provided the overdose has been take n within 10 \200\223 12 h, with methion- ine by mouth). Patients on enzyme-including drugs (e.g., carbamazepine, phenobarbital, phenytoin, rifampicin, alcohol) or who are malnourish ed (e.g., in anorexia, in alcoholism, or those who are HIV-positive) should be treated if t heir plasma-acetaminophen concentrations are above the high-risk treatment line (We thank D r. Alun Hutchings for permission to reproduce this graph.) 793 Burns Resuscitate and arrange transfer for all major burns. (>25% partial thick- ness in ad ult and >20% in children). Assess site, size, and depth of the burn. Referral is still warr anted in cases of full thickness burns >5%, partial thick- ness burns >10% in adults or >5% in children or the elderly, burns of special sites, chemical and electrical burns, and bur ns with inhalational injury. Assessment Burn size is important to assess (see Figure 20.4) as it influences the magnitude of the inflammatory response (vasodilatation, \206\221 vasc ular permeability) and thus the fluid shift from the intravascular volume. The size must be estimated to calculate fluid requirements. Ignore erythema. Burn depth determines healing time/scarring; assessing this may be difficult, even when experienced. The big distinction is whether the burn is partial thickness (painful, red, and blistered) or full thickness (i nsensate/painless and white/gray). NB: Burns can evolve, particularly over the first 48 h. Resuscitation Airway: Beware of upper airway obstruction developing if hot gasses inhaled. See Table 20.28. Suspect if history of fire in enclosed space, soot in oral/nasal cavity, s inged nasal hairs, or hoarse voice. A flexible laryngeo/bronchoscopy is useful. Involve ane sthesiologist early and consider early intubation. Breathing: Exclude life-threatening ches t injuries (e.g., tension pneumotho- rax) and constricting burns. Give 100% O 2 if carbon m onoxide poison- ing is suspected (mostly from history; may have cherry-red skin. Measure ca rboxyhemoglobin (COHb) and compare to nomograms. With 100% O 2 , t of COHb falls from 25 0 min to 40 min (consider hyperbaric oxygen if pregnant; CNS signs; >20% COHb). SpO2 measur ed by pulse oximeter is unreliable. Do escharotomy if thoracic burns impair chest excursion . Circulation: Partial thickness burns >10% in a child and >15% in adults re- quire IV flui d resuscitation. Insert two large-bore (14 or 16 g) IV lines. Do not worry if you have to p ut these through burned skin; intraosseous ac- cess is valuable in infants. Secure them wel l: They are literally lifelines. Use a burns calculator flow chart or a formula, such as th e Parkland formula (popular): 4 \227 weight (kg) \227 % burn = mL lactated Ringer \200 \231s in 24 h, half given in first 8 h. Modi \201 ed Brooke formula: 2 mL/kg for each % bu rn = ml lactated Ringer \200\231s in 24 h. Either formula is acceptable and the modified Br ooke has been shown to require less fluids without increasing harm. Replace fluid from the time of burn, not from the time first seen in hospital. See Figure 20.4. Formulas are only guides : Adjust IV infusion according to clinical response and urine output; aim for >0.5 m L/kg/h (>1 mL/kg/h in children), 50% more in electrical burns and inhalation injury. Monit or temperature (core and surface); catheterize the bladder. Treatment Do not apply cold wat er to extensive burns: This may intensify shock. If transferring to a burn unit, do not bur st blisters or apply any special creams as this can hinder assessment. Simple saline gauze or Vaseline gauze is suitable; cling movie is useful as a temporary measure and relieves pain. Use morphine in IV aliquots and titrate for good analgesia. Ensure tetanus immunity. Antibiotic prophylaxis is not routine. Definitive dressings There are many dressings for pa rtial thickness burns, including biological (pigskin, cadaveric skin), synthetic (Mepitel , DuoDERM ), and silver sulfadiazine cream (Flamazine ). Major full thickness burns benef it from early tangential excision and split-skin grafting as the burn wound is a major sour ce of inflammatory cytokines causing SIRS (systemic inflammatory response syndrome) and are an ideal medium for bacterial growth. 794 e n i c i d e m y c n e g r e m E Table 20.28 Smoke inhalation Initially, laryngospasm leads to hypoxia and straining (leading to pete- chiae), then hypox ic cord relaxation leads to true inhalation injury. Free radicals, cyanide compounds, and c arbon monoxide accompany thermal injury. Cyanide compounds (generated from burning plastic in particular) bind reversibly with ferric ions in enzymes, thus stopping oxidative phos- p horylation and causing dizziness, headaches, and seizures. Tachycardia and dyspnea soon giv e way to bradycardia and apnea. Carbon monoxide is generated later in the fire as oxygen is depleted; the COHb level does not correlate well with the severity of poisoning. \212 2 i s given to elute both cyanide and CO. \212 100% O Involve ICU/anesthesiologist early: Early ventilation may be useful; con- sider repe ated bronchoscopic lavage. Enroll expert help in cyanide poisoning. There is no single regi men suit- able for all situations. Clinically mild poisoning may be treated by rest, O 2 , and amyl nitrite 0.2 \200\2230.4 mL via an Ambu bag. IV antidotes may be used for moderat e poisoning: Sodium thiosulphate is a common first choice. More severe poisoning may requir e hydroxocobalamin, sodium nitrite, and dimethylaminophenol. \212 Figure 20.4 Lund & Browder charts 795