Investigations \212 \212 \212 \212 \212 \212 CXR(see X-RAY PLATES 5 and 8). Oxygen saturation, ABG if S CBC, CMP, LFT, CRP atypical sero logy Blood and sputum cultures Pleural fluid may be aspirated for culture Bronchoscopy and bronchoalveolar lavage if the patient is immunocom- promised or in ICU. a O 2 <92% or severe pneumonia Severity Core adverse features \200\234CURB \200\235 score: \212C onfusion \212B UN >20 mg/dL; \212R espiratory rate 30/min \212B P <90/60 mm Hg) A score >2 indicates severe p neumonia. Other features that increase the risk of death are age >50 yrs, coexisting diseas e, bilateral/multilobar involve- ment, P a O 2 <60 mm Hg or S a O 2 <92%. Management See Ta ble 20.13 Complications Pleural effusion, empyema, lung abscess, respiratory failure, septi cemia, pericarditis, myocarditis, cholestatic jaundice, renal failure. 766 e n i c i d e m y c n e g r e m E Table 20.13 Management of pneumonia Oxygen to maintain P a O 2 >60 mm Hg Caution if history of COPD \206\223 Treat hypotension and shock (p. 687) \206\223 Investigations \206\223 Antibiotics see Table 20.14 \206 \223 IV fluids may be required (anorexia, dehydration, shock) \206\223 Analgesia for pleur itic chest pain (e.g., acetaminophen 1 g/6 h or NSAID) \206\223 Some patients may need int ubation and a period of ventilatory support Table 20.14 Antibiotics Community-acquired Mild Doxycycline 100 mg/d PO, or Streptococcus Azithromycin 500 mg/d \227 3 d, 1 g then 500 mg/d \227 2 d or 2 g one time (all above pre ferred) or clarithromycin 1 g/d or 500 bid \227 7 d or levofloxacin 750 mg/d \227 7 d or moxifloxa- cin 400 mg/d \227 7 d pneumoniaeHae- mophilus influen- zaeMycoplasma pneumoniae Severe As above Levofloxacin 750 mg IV/PO or moxifloxacin 400 mg IV/PO q24h \227 7 \200\22310 days or (cef triax- one 1 g IV q24h or cefotaxime 1 g IV q8h each with azithromy- cin 500 mg/d IV/PO \227 3 days) Azithromycin 3 \200\2235 d or levofloxacin Atypical Legionella pneumophila Chlamydia species or moxifloxacin 7days Azithromycin or doxycycline 7 doxy 100 mg bid x High-dose co-trimoxazole Pneumocystis pneumoniae Hospital-acquired Gram +ve bacilli Pseudomonas Anaerobes If hospitalized >4 d, nursing home, ABX in last 90 d, immunosup- pression then vanc/linezol id for MRSA + antipseudomonal \222 -lactam + either (levoflox or Cipro) or (gent or tobra or amikacin). If none of the above features, then ceftriaxone 2 g/d IV or fluoroquinolone o r amp-sulbactam or ertapenem 767 (Continued) Table 20.14 (Continued) Aspiration Clindamycin q8h IV fluoroqui- Strep. pneumoniae nolone \227 10 d Anaerobes Massive pulmonary embolism Always suspect PE in sudden collapse 1 \200\2232 wks after surge ry. Mortality ranges from 0.7 to 6.0 per 100,000 persons. Mechanism Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood flow to lungs. The source is often occult. Risk factors \212 Malignancy \212 Surgery, especially pelvic \212 Immobil ity \212 Birth control pills (there is also a slight risk attached to HRT) \212 Previous thromboembolism and inherited thrombophilia Prevention Early postop mobilization is the sim plest method; consider: \212 \212 \212 \212 Antithromboembolic stockings Low-molecular-weight heparin prophylaxis SC Avoid contraceptiv e pill if at risk (e.g., major or orthopedic surgery). Recurrent PES may be prevented by an ticoagulation; vena caval filters are of limited use and should be combined with anticoagul ation. Signs and symptoms \212 \212 Acute dyspnea, pleuritic chest pain, hemoptysis, and syncope Hypotension, tachycardia, gall op rhythm, JVP heave, pleural rub, tachypnea, and cyanosis, AF \206\221 , loud P 2 , right ventricular Classically, PE presents 10 d postop with collapse and sudden breathlessness while strainin g at stool, but PE may occur after any period of immobility or with no predisposing factors . Breathlessness may be the only sign. Multiple small emboli may present less dramatically with pleuritic pain, hemoptysis, and gradually increasing breathlessness. Look for a source of emboli, especially DVT (is a leg swollen?). Investigations \212 \212 CBC, CMP, baseline clotting ECG(commonly normal or sinus tachycardia); right ventricular st rain pat- tern V1 \200\2233 (p. 95), right-axis deviation, RBBB, AF; may be deep S-waves in I, Q-waves in III, inverted T-waves in III ( \200\234S1 Q3 T3 \200\235) CXR is often norma l; increased vascular markings, small pleural effusion. Wedge-shaped area of infarction. \212 \212ABG: Hyperventilation + gas exchange \206\223 : P a O 2 \206\223 , P a CO 2 \206 \223 , pH often \206\221 \212 CT pulmonary angiography is sensitive and specific in determining if emboli are in pulmonar y arteries. If helical CT is unavailable, a ventilation \200\223 scan is equivocal, pul monary ) scan can aid diagnosis. If V perfusion (V angiography or bilateral lower ext ultra sound may help. D-dimer blood test, if low thrombosis absent. May help in excluding a PE. . /Q . /Q \212 768 e n i c i d e m y c n e g r e m E Table 20.15 Management of massive pulmonary embolism Oxygen, 100% \206\223 If critically ill, consider immediate surgery \206\223 IV access an d start heparin either unfractionated heparin 80 U/kg bolus then 18 U/kg/h IV as guided by aPTT or low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC q12h) \206\223 What is t he systolic BP? <90 mm Hg Start rapid fluid resuscitation If BP still \206\223 after 500 mL colloid, dobut amine 2.5 \200\22310 mcg/kg/min IV; aim for systolic BP >90 mm Hg If BP still low, consider norepinephrine If the systolic BP <90 mm Hg after 30 \200\22360 min of standard treatment and signs of right ventricular dilation on echo, clinically definite PE and no CI, consider thrombolysis. >90 mm Hg Start warfarin10 mg/24 h PO Confirm diagnosis Management See Table 20.15 for immediate management. \212 \212 Try to prevent further thrombosis with compression stockings. Heparin should be given for 3 d and until International Normalized Ratio (INR) >2. Then transition to warfarin. If obvio us remedial cause, 6 wks treatment with warfarin may be suffi- cient. Otherwise, continue f or at least 3 \200\2236 months (long-term if recurrent emboli or underlying malignancy). Is there an underlying cause (e.g., thrombophilic tendency), malignancy [especially prostate, breast, or pelvic cancer], SLE, or polycythemia)? If good story and signs, make the diagno sis. Start treatment before definitive investigations. \212 \212 Acute upper GI bleeding Causes Common : Gastric/duodenal ulcer, gastritis, Mallory \200\223 Weiss tear (esophageal tear due to vomiting), esophageal varices, portal hypertensive gastr opathy, drugs (NSAIDS, aspirin, thrombolytics, anticoagulants). Rarer: Hemobilia, nose blee ds (swallowed blood), esophageal/gastric malig- nancy, esophagitis, angiodysplasia, hemangi omas, Ehlers \200\223Danlos or Peutz \200\223 Jeghers syndrome, bleeding disorders, aorto-e nteric fistula (in those with an aortic graft). 769 Signs and symptoms Hematemesis or melena, dizziness (especially postural), fainting, abdomi nal pain, dysphagia? Postural hypotension, hypotension, tachycardia (not if on \222 -block er), \206\223 urine output, cool and clammy, signs of chronic liver disease; telangiectasi a or purpura; jaundice (biliary colic + jaundice + melena suggests hemobilia). NB: Ask abou t previous GI problems, drug use, and alcohol intake. Management Assess whether patient is in shock: \212 Cool and clammy to touch (especially nose, toes, fingers); refill Pulse >100 bpm Systolic B P <100 mm Hg Postural drop Urine output <30 mL/h \206\223 capillary \212 \212 \212 \212 If not in shock: Insert two big cannulae; start slow saline IV to k eep lines patent; check bloods and monitor vital signs + urine output. Aim to keep hemoglob in (HG) >8 g/dL. NB: HG may not fall until circulating volume is restored. If in shock: See Table 20.16 for management Variceal bleeding: Resuscitate, then proceed to urgent endoscop y for band- ing or sclerotherapy. Give octreotide 50 mcg/h IV infusion for 2 \200\2235 d. I f massive bleed or bleeding continues, pass a Sengstaken \200\223Blakemore tube. Pantoprazo le 40 mg IV may also be helpful in preventing stress ulceration. Endoscopy Within 4 h, if y ou suspect variceal bleeding; within 12 \200\22324 h if hypotensive on admission or signifi cant comorbidity. Endoscopy can identify the site of bleeding, estimate the risk of rebleed ing (rebleeding doubles mortality), and can be used to administer treatment. Risk of reblee ding: Active arterial bleeding seen (90% risk); visible vessel (70% risk); adherent clot/bl ack dots (30% risk). No site of bleeding identi \201 ed: Bleeding site missed on endoscopy ; bleeding site has healed (Mallory \200\223Weiss tear); nose bleed (swallowed blood); site distal to third part of the duodenum (Meckel diverticulum, colonic site). Rebleeds Serious event : 40% of patients who rebleed will die. If at-risk, maintain a high index of suspici on. If a rebleed occurs, check vital signs every 15 min and call senior cover. To prevent r ebleeding in endoscopically proven high-risk cases, IV pantoprazole has been tried (e.g., 8 0 mg followed by an infusion of 8 mg/h for 72 h). Signs of a rebleed: Rising pulse rate \212 \212 Falling JVP \212 Hematemesis or melena Fall in BP(a late and sinister findin g) and reduced consciousness level \212 Acute drug therapy Following successful endoscopic therapy in patients with major ulcer bleeding, IV pantoprazole (80 mg stat followed by 8 m g/h for 72 h) is recommended. There is no firm evidence to support the use of somatostatin or antifibrinolytic therapy in the majority of patients. \206\223 hourly urine output 770 e n i c i d e m y c n e g r e m E Table 20.16 Immediate management if hypotensive with GI bleed Protect airway and keep NPO \206\223 Insert two large-bore cannulae 14 \200\22316 g \206 \223 Draw bloods CBC, CMP, LFT, glucose, clotting screen Cross-match 6 units \206\223 Give high-flow O 2 \206\223 Rapid IV crystalloid infusion Up to 1 L \206\223 If remains hypot ensive, give blood Group specific or O Rh \200\223ve until cross-match done \206\223 Othe rwise slow saline/lactated Ringer \200\231s infusion a to keep lines open \206\223 Transfu se as dictated by hemodynamics \206\223 Correct clotting abnormalities Vitamin K, fresh fr ozen plasma (FFP), platelet concentrate \206\223 Set up CVP line to guide fluid replacemen t Aim for >5 cm H 2 O; CVP may mislead if there is ascites or CHF \206\223 Catheterize and monitor urine output Aim for >30 ml/h \206\223 Monitor vital signs every 15 min until sta ble, then hourly \206\223 Consider GI and/or surgery consult for all serious bleeds \206 \223 Urgent endoscopy for diagnosis control of bleeding Poor prognostic signs: \212 \212 \212 \212 Age >60 Systolic BP <100 mm Hg Bradycardia or rate >100 bpm Bleeding diathesis \212 \212 \212 Chronic liver disease Consciousness level \206\223 Significant comorbidity a Avoid saline in patients with decompensated liver disease (ascites, peripheral edema) as it wors- ens ascites, and, despite a low serum sodium, patients have a high body sodium. Us e whole blood or salt-poor albumin for resuscitation and 5% dextrose for maintenance. 771 Acute liver failure Fulminant liver failure is assumed to be potentially reversible. Theref ore, treatment is supportive and designed to buy time for the patient \200\231s liver to re generate. Management \212 Seek expert help. Is transfer to a ICU appropriate? Consider 20-degree head-up tilt in ICU. Treat the cause if known (e.g., acetaminophen overdose). Use caution with secretions and b lood if is hepatitis suspected. Check blood glucose q1 \200\2234h and give 50 mL 50% dextro se IV if <3.5 mmol/L. Give 10% dextrose IV, 1 L/12 h to avoid hypoglycemia. NGT to avoid as piration and remove any blood (bleeding varices) from stomach. Protect the airway with an e ndotracheal tube. Monitor temperature, pulse, respiratory rate (RR), BP, pupils, urine outp ut. Daily lab blood glucose, INR, CMP, LFT, ammonia, blood cultures, and EEG. The INR (or p rothrombin time [PT]) is the best measure of liver synthetic function. Avoid FFP unless ble eding or undergoing a surgical procedure. Some cen- ters give vitamin K daily. Platelet tra nsfusions may be required if throm- bocytopenic and bleeding. Daily weights (ascites) Minim ize absorption of nitrogenous substances and worsening of coma by restricting protein and e mptying the bowel with lactulose and magne- sium sulfate enemas. Aim for two soft stools pe r day. Consider neomycin 1 g/6 h PO to reduce numbers of bowel organisms. Consider N-acetyl cysteine. Even in nonacetaminophen liver failure, this can improve oxygenation and clotting profiles. Watch renal function carefully. Consider hemodialysis if water overload or acute renal failure develops. Reduce acid secretion and risk of gastric stress ulcers; e.g., wit h cimeti- dine, ranitidine IV or a proton pump inhibitor (e.g., pantoprazole). Avoid sedati ves (but diazepam is used for seizures) or other drugs with hepatic metabolism. Treat sepsi s aggressively and don \200\231t forget the risk of spontaneous bacte- rial peritonitis. \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 NB: Caution should be used when attempting to correct acid \200\223base imbalance as interv entions can sometimes be more harmful than anticipated. Meningitis Do not delay treatment; it may save a life. Make sure the referring physician gi ves a dose of antibiotic before sending the patient to you if possible. Presentation \212 Headache Meningismus: Neck stiffness, photophobia, Kerning \200\231s sign, Brudzinski \200 \231s \212 sign, headache, Jolt test positive (move the head quickly from side to side cau sing worse headache) Conscious level decreased; coma Petechial (nonblanching) rash; may onl y be one or two spots Seizures ( 20%) Focal neurological signs ( 20%) \212 \212 \212 \212 Common organisms \212Meningococcus \212Pneumococcus 772 \212Haemophilus influenzae (especially children) \212Listeria monocytogenes. Management \212 e n i c i d e m y c n e g r e m E Pay attention to the neurological exam; look for Careful examination: rashes; assess GCS. If hypotensive, resuscitate with fluids and oxygen . If intracranial pressure (ICP) is raised, summon help immediately and inform neurosurgeon s. Start antibiotics (below) immediately. \212 \212 \212 Investigations \212 \212 CMP, CBC, LFT, glucose, coagulation screen Blood culture, throat swabs (one for bacteria, o ne for virology), stool culture for viruses Lumbar puncture if safe. Don \200\231t forget t o measure the opening pressure! Contraindications are suspected intracranial mass lesion, f ocal signs, papilledema, trauma, or middle-ear pathology; major coagulopathy. Send samples for cell count and differential, C+S, Gram stain, protein estima- tion, glucose, and to vir ology. See Table 20.17. CT head before LP if mass lesion or raised ICP is suspected. CXR \212 \212 \212 Antibiotics Local policies vary. If in doubt, ask. The following are suggestion s only, when the organism is unknown: \212 <50 yrs: Vancomycin 1 g IV/12 h + ceftriaxone 2 g IV over >2 min as 1 daily dose. >50 yrs: Vancomycin 1 g IV/12 h + ceftriaxone 2 g IV over >2 min daily + ampicillin 2 g IV/4 h (for Listeria ). Acyclovir if herpes encephalitis is suspected. Once organism is isolated, seek urgent microbiological advice. \212 \212 \212 Further measures \212 There is some evidence that high-dose steroids may reduce neurological complications. There fore, some centers recommend the administration of dexamethasone 10 mg IV before or with th e first dose of antibiotics (but do not delay giving antibiotics), then q6h for 4 d. Avoid in patients with shock. General supportive measures Remember, meningitis is a notifiable di sease. Inform local public health officer for contact tracing. Antibiotic prophylaxis for f amily and close contacts (depends on the organism: Ask a microbiologist) \212 \212 \212 \212 Table 20.17 Typical CSF in meningitis Pyogenic Often turbid Tuberculous Often fibrin web Mononuclear 10 \200\2231,000/mm 3 Viral ( \200\234aseptic \200\235) Usually clear Appearance Predominant cell Polymorphs White Cell Mononuclear 50 \200\2231,000/mm 3 e.g., 90 \200\2231,000+ count/mm3 < plasma >1.5 In smear and culture Often absent in < plasma 1 \200\2235 > plasma <1 Not in smear or culture Glucose Protein (g/l) Organisms 773 smear (There are no hard-and-fast rules) Cerebral abscess Suspect this in any patient with elevated ICP, especially if there is feve r or elevated WBC. It may follow ear, sinus, dental, or periodontal infection; skull fractu re; congenital heart disease; endocarditis; bronchiectasis. Signs: Seizures, fever, localiz ing signs, or signs of elevated ICP. Coma. Signs of sepsis elsewhere (e.g., teeth, ears, lu ngs, and endocarditis). Investigations: CT/MRI(e.g., \200\234ring-enhancing \200\235 lesio n), \206\221 WBC, \206\221 ESR, biopsy. Treatment: Urgent neurosurgical referral; treat \206\221 ICP. If frontal sinuses or teeth are the source, the likely organism will be Strep . milleri (microaero- philic) or oropharyngeal anaerobes. In ear abscesses, B. fragilis or other anaerobes are most common. Bacterial abscesses are often peripheral; Toxoplasma lesio ns are deeper (e.g., basal ganglia). Consider the possibility of underlying immunosuppressi on. Status epilepticus Seizures lasting for >30 min or repeated seizures without intervening co n- sciousness. Mortality and the risk of permanent brain damage increases with the length o f attack. Aim to terminate seizures lasting more than a few minutes as soon as possible (<2 0 min). Status usually occurs in known epileptics. If it is the first presentation of epile psy, the chance of a structural brain lesion is high (>50%). Diagnosis of tonic \200\223clo nic status is usually clear. Nonconvulsive status (e.g., absence status or continuous parti al seizures with preservation of consciousness) may be more difficult: Look for subtle eye or lid movement. An EEG can be very helpful. Could the patient be pregnant (any pelvic mass )? If so, eclampsia is the likely diagnosis; check the urine and BP: Call a senior obstetri cian \200\224 immediate delivery may be needed. Investigations \212 Bedside glucose; the following tests can be done once treatment has started: Glucose, blood gasses, CMP, Ca 2+ ,CBC, ECG Consider anticonvulsant levels, toxicology screen, LP, cultur e blood and urine, EEG, CT, carbon monoxide level Pulse oximetry, cardiac monitor \212 \212 Treatment See Table 20.18. Basic life support and these agents: Lorazepam 2 mg as a slow bolus (over 2 min) into a large vein. Beware respiratory arrest during the last part o f the injection. Have full resuscita- tion facilities at hand for all IV benzodiazepine use . ( Alternative: Diazepam, but it is less long-lasting; give 10 mg IV over 2 min; if needed , repeat at 5 mg/min, until seizures stop, or 20 mg given, or significant respiratory depre ssion occurs.) The rectal route is an alternative for diazepam if IV access is difficult. W hile waiting for this to work, prepare other drugs. If seizures continue: fosphenytoin infu sion: 15 \200\22320 mg PE/kg IV, at a max rate of 150 mg/min. (Don \200\231t put diazepam i n same line: They don \200\231t mix.) Beware BP \206\223 and do not use if bradycardic or heart block. Requires BP and ECG monitoring. 100 mg/q6 \200\2238h is a maintenance dose (ch eck levels). If seizures continue: Dexamethasone 10 mg IV if vasculitis/cerebral edema (tum or) is possible. General anesthesia expert guidance on ICU. 774 As soon as seizures are controlled, start oral drugs. Ask what the cause was (e.g., hypogly cemia, pregnancy, alcohol, drugs, CNS lesion or infection, hypertensive encephalopathy, ina dequate anticonvulsant dose). e n i c i d e m y c n e g r e m E Table 20.18 Management of status epilepticus Open and maintain the airway, put patient in recovery position Remove false teeth if poorly fitting, insert oral/nasal airway, intubate if necessary \206\223 Oxygen, 100% + suction (as required) \206\223 IV access and take blood CMP, LFT, CBC, glucose, calcium, Toxicolog y screen if indicated, anticonvul- sant levels \206\223 Thiamine 100 mg IV over 10 min if alcoholism or malnourishment suspected. Unless glucose known to be normal IV glucose 50 mL 50% \206\223 Correct hypotension with fluids \206\223 Slow IV bolus phase to stop seizure s: E.g., lorazepam 2 \200\2234 mg, or Diazepam 10mg with 5mg/min repeat to total of 20mg \206\223 IV infusion phase: If seizures continue, start phenytoin,15 mg/kg IV, at a rate of 50 mg/min or fosphenytoin at 15 \200\22320 mg PE/kg at rate of 150 mg PE/min. Monitor ECG and BPP. 100 mg/q6 \200\2238h is a maintenance dose (check levels). \206\223 General anest hesia phase: Continuing seizures require propofol drip versus expert help with paralysis an d ventilation with continuous EEG monitoring in ICU Never spend >20 min on someone with sta tus epilepticus without admission to the neurointensive critical care unit or similar type unit. Head injury If the pupils are unequal, diagnose rising ICP(e.g., from extradural hemor- rha ge) and summon urgent neurosurgical help. Retinal vein pulsation at funduscopy helps exclud e ICP \206\221 . Initial management (See Table 20.19.) Write full notes. Record times. \212 Involve neurosurgeons at an early stage, especially with comatose patients or if elevated I CP suspected. Examine the CNS. Chart pulse, BP, temperature, respirations + pupils every 15 min. Maintain c-spine immobilization until an adequate exam can be done. Assess antegrade amnesia (loss from the time of injury; i.e. post-traumatic) and retrograde amnesia \200\224 its extent correlates with the severity of the injury, and it never occurs without antegrad e amnesia. Provide meticulous care to bladder and airway. \212 \212 \212 \212 Who needs a CT head scan? If any of the following are present, a CT is required immed iately: \212 GCS <13 at any time, or GCS 13 or 14 at 2 h following injury \212 Focal neur ological deficit Suspected open or depressed skull fracture or signs of basal skull \212 f racture Post-traumatic seizure 775 \212 Suspicion of Alcohol or drug use \212 \212 Vomiting more than once Loss of consciousness \212 \212 \212 \212 or any of the following: Age 65 Coagulopathy \200\234Dangerous mechanism of injury \200\235 (e.g., fall from great height) Confusion When to ventilate immediately: \212 \212P a O 2 <70 mm Hg in air (<100 mm Hg with O 2 ) o r P a CO 2 >45 mm Hg \212 \212 Ventilate before neurosurgical transfer if: \212 Deterior ating level of consciousness \212 Bilateral fractured mandible \212 Bleeding into mouth ( e.g., skull base fracture) \212 Seizures Risk of intracranial hematoma in adults \212 Ful ly conscious, no skull fracture = <1:1,000 \212 Confused, no skull fracture = 1:100 \212 Fully conscious, skull fracture = 1:30 \212 Confused, skull fracture = 1:4 Criteria for ad mission \212 \212 \212 Coma 8 on GCS Spontaneous hyperventilation ( Respiratory irregularity. P a CO 2 <26 mm Hg) Difficult to assess (child, postictal, alcohol intoxication) CNS signs, severe headache or vomiting, fracture Loss of consciousness does well and a responsible adult is in attendance . not require admission if patient is otherwise Drowsy trauma patients (GCS <15 to >8) smelling of alcohol: Alcohol is an unlikely cause of coma if plasma alcohol <50 mg/dL. If unavailable, estimate blood alcohol level from the os molar gap. Never assume signs are just alcohol . Complications Early: Extradural/subdural h emorrhage, seizures. Late: Subdural; seizures, diabetes insipidus, parkinsonism, dementia. Indicators of a poor prognosis Increased age, decerebrate rigidity or any posturing, extens or spasms, prolonged coma, hypertension, hypoxemia, temperature >39 C. 60% of those with l oss of consciousness of >1 month will survive 3 \200\22325 yrs, but may need daily nursing care. 776 e n i c i d e m y c n e g r e m E Table 20.19 Immediate management plan for head injury ABC \200\231s \206\223 Oxygen, 100% Intubate and hyperventilate if necessary NB: Beware of a cervical spine injury \206\223 Stop blood loss and support circulation Treat for shock if required \206\223 Treat seizures with benzodiazepine \206\223 Assess level of consciou sness (GCS) Antegrade and retrograde amnesia \206\223 Rapid examination survey \206\223 I nvestigations glucose, CMP, CBC, blood alcohol, toxicology screen, ABG and clotting \206 \223 Neurological examination \206\223 Brief history When? Where? How? Had a fit? Lucid in terval? Alcohol? \206\223 Evaluate lacerations of face or scalp Palpate deep wounds with s terile glove to check for step deformity. Note obvious skull/facial fractures a \206\223 C heck for CSF leak from nose or ear Any blood behind the ear drum? If either is present, sus pect basilar skull fracture: Do CT Give tetanus toxoid and refer at once to neurosurgeons \206\223 Palpate the neck posteriorly for tenderness and deformity . If detected, or if the patient has obvious head injury or injury above the clavicle with loss of consciousness, i mmobilize the neck and get cervical spine radiographs \206\223 Radiology As indicated: Cer vical spine, CXR, CT of head a Periorbital \200\234raccoon sign \200\235 or postauricular Battle \200\231s sign ecchymo ses. 777 Raised intracranial pressure There are three types of cerebral edema: \212 Increased capillary permeability \200\224tumor, trauma, ischemia, Vasogenic: infection Cytotoxic: \212 \212Interstitial (e.g., obstructive hydrocephalus) Because the cranium defines a fix ed volume, brain swelling quickly results in \206\221 ICP, which may produce a sudden clin ical deterioration. Normal ICP is 0 \200\22310 mm Hg. The edema from severe brain injury is probably both cyto- toxic and vasogenic. Causes \212 \212 \212 Cell death from hypoxia Primary or metastatic tumors Head injury Hemorrhage intraventricular) Meningoencephalitis, brain abscess Hydrocephalus, cerebral edema, status epilepticus (subdural, extradural, subarachnoid; intracerebral, \212 \212 Signs and symptoms \212 \212 Headache, drowsiness, vomiting, seizures. History of trauma. Listlessness, irritability, dr owsiness, falling pulse and rising BP (Cushing \200\231s response), coma, Cheyne \200\223St okes respiration, pupil changes (constriction at first, later dilatation \200\224do not mas k these signs by using agents such as tropicamide to dilate the pupil to aid funduscopy). P apilledema is an unreliable sign, but venous pulsation at the disc may be absent (absent in 50% of normal people, but loss of it is a useful sign). \212 Investigations \212 CMP, CBC, LFT, glucose, serum osmolality, clotting, blood culture, CXR CT head Then conside r lumbar puncture, if safe. Measure the opening pressure! \212 \212 Treatment The goal is to lower ICP and avert secondary injury. Urgent neurosurg ery is required for the definitive treatment of \206\221 ICP from focal causes (e.g., hema tomas). This is achieved via a craniotomy or burr hole. Also, an ICP monitor (or bolt) may be placed to monitor pressure. Surgery is generally not helpful following ischemic or anoxi c injury. Holding measures are listed in Table 20.20. Herniation syndromes Uncal herniation is caused by a lateral supratentorial mass that pushes the ipsilateral inferomedial tempor al lobe (uncus) through the temporal incisura and against the midbrain. The third nerve, tr aveling in this space, is compressed, causing a dilated ipsilateral pupil, then ophthalmopl egia (a fixed pupil localizes a lesion poorly but is \200\234ipsi-lateralizing \200\235). This may be followed (quickly) by contralateral hemiparesis (pressure on the cerebral pedun cle) and coma from pressure on the ARAS in the midbrain. Cerebellar tonsil herniation is ca used by increased pressure in the posterior fossa forcing the cerebellar tonsils through th e foramen magnum. Ataxia, VI nerve palsies, and +ve Babinski (upgoing plantars) occur first , then loss of con- sciousness, irregular breathing, and apnea. This syndrome may proceed v ery rapidly given the small size of and poor compliance in the posterior fossa. Subfalcine (cingulate) herniation is caused by a frontal mass. The cingulate gyrus (medial frontal lob e) is forced under the rigid falx cerebri. It may be silent unless the anterior cerebral ar tery is compressed and causes a stroke; e.g., contralateral leg weakness abulia (lack of decision-making). 778 e n i c i d e m y c n e g r e m E Table 20.20 Immediate ICP management plan ABC \200\231s \206\223 Correct hypotension and treat seizures \206\223 Brief examination, history if available Any clues (e.g., meningococcal rash, previous carcinoma) \206\223 El evate the head of the bed to 30 \200\22340 degrees \206\223 If intubated, hyperventilate t o \206\223 P a CO 2 (e.g., to 26 mm Hg) This causes cerebral vasoconstriction and reduces ICP almost immediately \206\223 Osmotic agents (e.g., mannitol) can be useful but may lead to rebound \206\221 ICP after prolonged use ( 12 \200\22324 h) Give 20% solution 1 \200 \2232 g/kg IV over 10 \200\22320 min (e.g., 5 ml/kg). Clinical effect is seen after 20 min and lasts for 2 \200\2236 h. Follow serum osmolality \200\224aim for 300 mosmol/kg but do n \200\231t exceed 310 \206\223 Corticosteroids are not effective in reducing ICP except f or edema surrounding tumors (e.g., dexamethasone 10 mg iv and follow with 4 mg/6 h IV/PO) \206\223 Restrict fluid to <1.5 L/d \206\223 Monitor the patient closely, consider monitor ing ICP \206\223 Aim to make a diagnosis \206\223 Treat cause or exacerbating factors (e. g., hyperglycemia, hyponatremia) \206\223 Definitive treatment if possible Diabetic ketoacidosis Hyperglycemic ketoacidotic (DKA) coma occurs mainly in type 1 diabete s: It may be the initial presentation for a newly diagnosed diabetic patients. Precipitants include infection, surgery, MI, noncompliance, or wrong insu- lin dose. The diagnosis requ ires the presence of ketosis and metabolic acidosis. Signs and symptoms \212 Polyuria, polydipsia, lethargy, anorexia, hyperventilation, ketotic breath, dehydration, vo miting, abdominal pain, coma Investigations \212 3, amylase, osmolality, ABG, CBC, urine and Lab glucose, CMP, HCO blood cultures, serum ketones Urine tests: Ketones, CXR To estimate plasma osmolarity: 2[Na mg/dL]/18 \212 \212 + ] + [(urea) mg/dL]/2.8 + [(glucose) 779 Key points in the treatment of diabetic ketoacidosis Treat dehydration aggressively with IV F. \212 is usually high, but not always, especially when insulin Plasma glucose therapy is instituted. High WBC Infection: Start broad-spectrum antibiotics early if infection is suspected. \212 \212 may be seen in the absence of infection. Often there is no fever. Do urine and blood cultures and CXR. \212Hyponatremia: Pseudohyponatremia is common due to osmolar compen- sation for the hyper glycemia. Corrected plasma [Na + ] = measured Na + 1.6 (Glucose \200\223 100) Blood glucos e may return to normal long before ketones Ketoacidosis: are cleared from the bloodstream. A rapid reduction in the amount of insulin administered in response to a decrease in serum glucose may lead to lack of clearance and return to DKA. This may be avoided by maintain- i ng a constant rate of insulin (e.g., 0.1 U/kg/h IV) and co-infusing D5W to when plasma gluc ose falls below 250 \200\223300 mg/dL during the extended insulin regimen. \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