Table 3.4 CURB-65 score for pneumonia Score Confusion 1 Urea > 7mmol/L 1 Respiratory rate \211 30/min 1 Low BP (systolic <90mmHg or diastolic \211 60mmHg) 1 Age \211 65 years 1 Treatment Patients deemed suitable for discharge Provide simple analgesia, oral antibiotics , and GP follow-up. Patients admitted, but not severely unwell Start either oral or IV antibiotics, as follows: \200 Either amoxicillin 0.5 \200\2231g PO tds + erythromycin 500mg PO qds (or clarithromycin 500mg bd). Or if IV therapy is needed: ampicillin 500mg IV qds + erythromycin 500mg IV qds (or clarith romycin 500mg bd). Local guidelines will apply. Monitor SpO 2 and provide O 2 accordingly. \200 Provide simple analgesia. Patients with s epsis or severe sepsis (see b p.59) Commence IV crystalloid \202 uids, take blood culture s and administer IV antibiotics (eg co-amoxiclav 1.2g IV tds + clarithromycin 500mg IV bd) immediately. Contact ICU and make preparations for arterial line, central line and urinary catheter insertion. Aim for CVP > 8mmHg, MAP > 65mmHg and urine output > 0.5mg/kg/hr. See s evere sepsis guidelines ( www. surviving sepsis.org ). Differential diagnosis Pneumonia-like presentations can occur with pulmonary oedema, pulmon ary infarction, pulmonary vasculitis (eg SLE, PAN, Churg \200\223Strauss and Wegener \200 \231s), aspergillosis, allergic alveolitis, bronchial or alveolar cell carcinoma, acute pan creatitis, and subphrenic abscess. 112 CHAPTER 3 Medicine Pulmonary aspiration Aspiration of solid or liquid material into the upper and lower airway s is likely when one or more of the following features are present: \200 d GCS : head inj ury, stroke, overdose, seizures, sedation, anesthesia. \200 d Cough and/or gag re \202 e xes : related to above factors and/or bulbar dysfunction, intubation/extubation, Guillain \200\223Barr syndrome, multiple sclerosis, myasthenia gravis. Tendency to regurgitate/vomit: alcohol, full stomach, upper GI tract pathology (including h iatus hernia, oesophageal obstruction, pregnancy). May occur in in \201 rm or elderly fed via nasogastric tube. Clinical features Large food particles suf \201 cient to cause complete airway obstruction cause choking, inability to speak, i respiratory effort, cyanosis, loss of consciousness, and death. Smaller particles may pass through the vocal cords causing coughing, stridor, ta chypnoea, and wheeze. 80 % of patients are aged <4 years, with peanuts being the classic in haled objects. Delayed presentation with cough, wheeze, haemoptysis, unresolved pneumonia, abscess formation, or empyema occurs in 830 % often days or weeks later. Vomiting/regurgita tion is often witnessed and pulmonary aspiration con \201 rmed by seeing gastric contents in the oropharynx or trachea during intubation or following suction. Gastric content is a m ixture of semi- solid and liquid material \200\224 aspiration leads to a sudden onset of s evere dypsnoea, wheeze, and cyanosis. Its acid nature causes severe damage to the alveolar- capillary membrane, with denaturation of pulmonary surfactant, i pulmonary permeability wit h oedema and atelectasis. Hydrocarbons (eg gasoline, paraf \201 n) cause severe pulmonary toxicity if aspiration occurs during ingestion or following regurgitation/vomiting. Investigations ABG These show hypoxaemia within minutes of acid aspiration. Initially, pati ents may hyperventilate with d pCO 2 until pulmonary compliance i work of breathing suf \201 cient to result in hypoventilation. CXR Abnormalities develop in > 90 % of patients, but may take hours/days. Appearances depen d on the nature of the aspirated material and the patient \200\231s position at the time of the episode (right lower lobe is most frequently and severely affected, followed by left l ower lobe and right middle lobe). In severe aspiration, diffuse bilateral in \201 ltrates and pulmonary oedema similar to ARDS appearances are present. Less severe episodes produce atelectasis followed by alveolar in \201 ltration. Intrapulmonary foreign body (including peanuts) Rarely radio-opaque. Resulting collapse, hy perin \202 ation, or consolidation is usually obvious and depends on whether obstruction i s complete or partial and if supervening infection is present. If the history strongly sug- gests an inhaled FB, but CXR is normal, consider an expiratory CXR, which may show evidenc e of air trapping distal to the obstruction. 113 PULMONARY ASPIRATION Prevention Prevention is everything. Pay meticulous attention to airway protection. This ma y involve positioning (tilt head down on the right hand side), suction to the oropharynx (Y ankauer catheter avoiding stimulation of the gag re \202 ex) and if necessary, tracheal in tubation. Tracheal intubation does not completely protect against aspiration of \202 uid into the lungs, but it is the best preventative measure. In at-risk patients, pass an NG tu be to empty the stomach. However, NG tubes can also predispose to aspiration by preventing closure of the oesophageal sphincters and interfering with coughing and clearing the pharyn x. Treatment Correct hypoxia and give nebulized salbutamol for associated bronchospasm. If par ticulate aspiration is present, refer for urgent bronchoscopy. Although secondary infection is common, the use of antibiotics or steroids is not routinely indicated. 114 CHAPTER 3 Medicine Spontaneous pneumothorax Primary spontaneous pneumothorax (PSP) may occur in previously hea lthy individuals. Secondary spontaneous pneumothorax (SSP) occurs in older patients with pr e-existing chronic lung disease (like COPD or TB) and may also occur with asthma, bronchial carcinoma, Marfan \200\231s syndrome, infection, cystic \201 brosis, and oesophageal rup ture. Presentation Most patients present with unilateral pleuritic chest pain and dyspnoea. Class ical physical signs may not be present (depending upon the size of the pneumothorax): tachy pnoea, tachycardia, normal/hyper-resonant per- cussion note withe d air entry on the affect ed side. Rarely, there may be a clicking sound at the cardiac apex. Severe symptoms (inabil ity to speak, gasping, low SpO 2 ) should prompt rapid assessment tracheal deviation, tachy pnoea, tachycardia, and hypotension. Treat tension with immediate decompression using a nee dle in the second intercostal space (just above the third rib) in the mid-clavicular line ( b p.328). Severe symptoms are also found in patients with SSP (disproportionate to the pne umothorax size). In the absence of signs of tension pneumothorax, obtain an emergency porta ble CXR and involve an experienced doctor. for tension pneumothorax: Investigation and treatment \200 Monitor pulse, SpO 2 , and BP. Ensure IV access. \200 Administer high \202 ow oxygen (aim SpO 2 90 \200\22392 % in patients with COPD). When there are no signs of tension, an ABG will help assess patients with chronic lung disease, and guide oxygen therapy. Erect CXR \200 When using digital images, always use a picture archiving and communi- cat ion system (PACS) workstation. The signs of pneumothorax may be subtle and dif \201 cult t o spot. Look for a displacement of the pleural line. \200 Do not mistake the scapular edge for th e lung edge. \200 Some patients with COPD have emphysematous bullae, which can mimic pneu mothorax. If in doubt, ask for senior review prior to treating for pneumothorax. An air \202 uid level at the costophrenic angle may be present. CT scan Can be of use in the sub-acute setting for assessing bullous lung disease in a stable patient. CT is not a p rimary diagnostic modality. Intervention \200 Should be guided primarily by the patient \200\231s symptoms. If the pa tient is breathless, they should undergo an intervention. The size of the pneumothorax can be estimated on CXR by measuring from the chest wall to th e lung edge at the level of the hilum. This is 115 SPONTANEOUS PNEUMOTHORAX only an estimate and assumes symmetrical lung collapse. The cut-off of 2cm is used to deter mine treatment. Intervention for PSP is needle aspiration. If unsuccessful, do not repeat aspiration. Instead insert a Seldinger chest drain. Treatment for symptomatic SSP is chest drain insertion and admission. \200 Treatment for SSP without breathlessness is admission. Aspiration should be performed by an experienced d octor and may require CT. Always insert chest drains for bilateral pneumothoraces. \200 Always insert a chest drain immediately following emergency needle decompression. Pleural aspiration and drain insertion should be performed by a doctor who has prior training and experience. Ensure the patient has IV access. Perform in a monitored environment with an assistant and appropriate supervision. Use aseptic technique. \200 Always discuss the procedure with th e patient and document that they have given their consent. If the patient is on anticoagulation or has a known coagulopathy dis- order, discuss with a haemotologist \201 rst. Aspiration technique Con \201 rm the side of the pneumothorax. Sit the patient upright. In \201 ltrate 1 % lidocaine, then insert a 16G IV cannula just above the 3rd rib (in the 2n d intercostal space) in the mid-clavicular line. Alternatively, lay the patient on their si de with the pneumothorax side upwards. Insert cannula in the 5 th intercostal space, in the anterior axillary line. Remove the needle, attach a three-way tap, then aspirate air with a 50mL syringe. Continue aspiration until the patient coughs excessively, or until 2.5L of air is removed. Seldinger chest drain insertion Con \201 rm the side of the pneumothorax. Keep the patient comfortable, ensure adequate analgesia (this may require 1mg increments of morphine IV), b ut avoid sedation. Sit the patient upright and rest their hand behind their head. In \201 ltrate 10mL 1 % lidocaine at the anterior axillary line in the 5th inter- costal space. Asp irate a small amount of pleural air during in \201 ltration and note the depth of the pleu ral space. Locate the pleural space with the intro- ducer needle (aspirate while advancing through chest wall), then advance the guidewire through the needle. Remove the introducer n eedle, make a small skin incision and gently pass the dilator over the guidewire using a tw isting action. Do not push the dilator more than 1cm past the depth of the pleural space. P ass the chest drain over the guide wire to a depth of 10 \200\22312cm. Remove the guide wir e, connect to an underwater seal drain and suture in pace. Check the drain is bubbling and swinging, and organize a CXR. Discharge Patients without breathlessness, with small PSP may be considered for discharge. Give the patient verbal and written instructions to return if their symptoms worsen and war n them not to \202 y. Ensure they have an appointment with a respiratory physician in the next week. See http://www.brit-thoracic.org.uk 1 1 6 Spontaneous pneumothorax If bilateral/haemodynamically unstable proceed to chest drain C H A P T E R Age >50 and significant smoking history evidence of underlying lung disease on exam or CXR? 3 NO YES Secondary pneumothorax Primary pneumothorax M e d i c i n e YES >2 cm or breathless Size >2 cm and/or breathless Aspirate 16 \200\22318G cannula aspirate <2.5L YES* NO NO Aspirate 16 \200\22318G cannula aspirate <2.5L YES Size 1 \200\2232 cm Success (<2 cm and breathing improved) NO YES NO Success size now <1 cm Consider discharge review in OPD in 2 \200\2234 weeks NO YES Chest drain Size 8 \200\22314Fr admit In some patients with a large pneumothorax but minimal symptoms conservative management may be appropriate Admit high flow oxygen (unless suspected oxygen sensitive) observe for 24 hours Fig. 3.23 Management of pneumothorax. 1 1 Thorax 2010; 65 (Suppl 2): ii18eii31. doi:10.1136 /thx.2010.136986. This page intentionally left blank 118 CHAPTER 3 Medicine Deep venous thrombosis DVT and PE are manifestations of the same disease process whereby ab normal clotting occurs in the veins of the legs or pelvis. The clots may break from the vei n wall and embolize to the lungs. Untreated DVTs are associated with a 1 \200\2232 % mortal ity from PE. Around half of those with DVT will go on to develop post-thrombotic syndrome, with lifelong pain and swelling of the leg. Risk factors \200 Recent surgery (where a general anesthetic was administered, espe- cially orthopedic, abdominal, spinal and obstetric). Recent admission to hospital. \200 Current malignancy. \200 Being bedbound. \200 Seps is. \200 IV drug use (where patient injects in the femoral vein). \200 Pregnancy/pelvic masses. \200 Immobility such as recent fracture with crutches and plaster cast. \200 P revious DVT/PE. \200 Thrombophilia or family history of venous thromboembolism. Clinical features DVT classically produces leg pain with swelling, warmth, tenderness, and dilated super \201 cial veins in the affected leg. These signs are non-speci \201 c and o ften not present. A small or partially occluding thrombus may be completely asymptomatic. H istory and clinical examination alone cannot safely exclude DVT \200\224 if a DVT is suspe cted, investigate further. Investigate for PE, rather than DVT if the patient has tachycard ia, hypoxia, increased respiratory rate, or breathlessness ( b Pulmonary embolus, p.120). Differential diagnosis \200 Muscular tear: typically acute onset. \200 Rupture of a Bak er \200\231s cyst: again, typically acute onset. \200 Cellulitis or other infection. Investigation and management \200 Record pulse rate, RR, BP, SpO 2 , and T in all pati ents. \200 Take a full history including concurrent illness, past history, recent operations, travel, and family history. Examine the affected leg for signs of plethora, deep vein tenderness, swelling (measure bot h legs, 10cm distal to tibial tuberosity), oedema and dilation of the skin veins. Perform full examination checking for signs of PE or occult carcinoma. \200 Calculate the clinical probability assessment score. The Wells score (Table 3.5 ) is the most widely used clinical prediction score. Take FBC, U&E, CRP, glucose. \200 Take D-dimer if Wells score indicates DVT is \200\230u nlikely \200\231 (<3 points). \200 If D-dimer normal and DVT \200\230unlikely \200\231, DVT has been ruled out. 119 DEEP VENOUS THROMBOSIS Table 3.5 Wells clinical probability assessment score for DVT Clinical feature Score Active cancer (treatment within 6 months or palliative care) 1 Paralysis, paresis, or recent POP immobilization of a leg 1 Recently bedridden for > 3 days or major surgery <12 weeks 1 Localized tenderness along the distribution of the deep venous system 1 Entire leg swelling 1 Calf swelling > 3cm compared with asymptomatic leg 1 Pitting oedema (greater in the symptomatic leg) 1 Dilated super \201 cial veins (non-varicose) 1 Previously documented DVT 1 Another diagnosis more likely than DVT 2 Total score < 3 means DVT is \200\230unlikely \200\231. Score of 3 or more signi \201 es DVT is \200\230likely \200\231. The Wells score was not developed with injecting drug users or pregnant women, both of whom are at higher risk of DVT. These patients should always undergo ultrasound scanning. All p atients investigated for DVT with a \200\230likely \200\231 Wells score ( \211 3) or an elevated D-dimer level require ultrasound scanning. A normal whole leg ultrasound scan (fem oral, popliteal, and calf vein scan) will exclude DVT. If a thigh scan is performed (the fe moral and popliteal veins), DVT can only be excluded by two normal thigh ultrasound scans, one week apart. All patients with a \200\230likely \200\231 score should be anticoagulated with LMWH while awaiting an outpatient ultrasound scan. Patients diagnosed with calf or thigh DVT should be treated with LMWH and discharged with a week \200\231s supply, an appointment for the anticoagulation services, and medical outpat ient follow-up. Advise them to return immediately if they become breathless or have chest p ain. Upper limb DVT Seen almost exclusively in patients with in-dwelling central or long lines, often for chemotherapy. May be associated with plethora and swelling of the arm or face. If suspected, request an ultrasound of the arm and neck veins, or a CT scan with contrast. Super \201 cial thrombophlebitis Patients present with a painful, tender area of skin. The diagnosis is made clinically with a \201 rm, tender super \201 cial vein, and overlying erythema. This may co-exist with DVT and super \201 cial thrombus may propagate into deep veins. If there is any doubt as to the presence of a DVT, investigate using the DVT protoc ol. Otherwise, treat with NSAID. Arrange follow up either in the ED, a medical clinic or wi th the GP. 120 CHAPTER 3 Medicine Pulmonary embolism The mortality of diagnosed and treated pulmonary embolism is 7 % . Many more people die from undiagnosed PE. Venous thromboembolism develops in patients already su ffering from sepsis, cancer, or COPD or in patients recovering from stroke, MI, surgery, an d joint replacement. Pulmonary embolic disease can result in a variety of symptoms often mi sdiagnosed as asthma, anxiety, pneumonia and ACS. History Most patients with PE experience dyspnoea, commonly without other symptoms. Syncope with cyanosis, cardiac arrest or angina are signs of massive PE. A minority present with p leuritic chest pain, some with additional haemoptysis. Always consider PE in patients with unexplained hypoxia or breathlessness. Take a full history of concurrent illness, surgical procedures, recent hospital admission, past history including DVT and PE, travel and family history. Examination Examination may be normal. \200 Tachycardia and tachypnoea are common. \200 Pyrexia following lung infarction is common. \200 30 % of all patients with PE have norm al SpO 2 . \200 Always record BP. Hypotension indicates massive PE. \200 Perform a full respiratory and cardiovascular examination. \200 Always examine the legs for signs of DV T. Table 3.6 Modi \201 ed Wells clinical probability assessment score for PE Clinical feature Score Signs of DVT (minimum of objective leg swelling and tenderness) 3.0 IV drug use 3.0 PE is the most likely diagnosis 3.0 HR > 100 1.5 Prior PE or DVT diagnosis 1.5 Bed ridden for > 3 days or surgery, within the past 4 weeks 1.5 Cancer (treated actively or with palliation within last 6 months) 1.0 Haemoptysis 1.0 Total score <2.0 = low risk PE, 2.0 \200\2236.0 = moderate risk PE, > 6.0 = high risk PE. Any patient scoring 2.0 or more on the Wells score, OR who has an elevated D-dimer, require s pulmonary imaging. Note that a normal D-dimer will not exclude PE in a patient with moder ate or high probability of PE. Only a normal D-dimer and a low clinical probability will sa fely exclude PE. 121 PULMONARY EMBOLISM Investigations for suspected pulmonary embolus \200 If hypoxic, tachycardic, or hypotensi ve, insert an IV cannula. \200 All patients should have blood taken for FBC and U&Es. \200 Take a D-dimer test on any patient who scores <2.0 on the Wells score (Table 3.6 ). N ormal D-dimer in a patient scoring <2.0 excludes PE. \200 Arrange ECG (to look for MI or pericarditis) and CXR (to look for pneumothorax, pneumonia). Many patients with PE have a n ormal ECG and CXR. Diagnostic imaging for pulmonary embolus There are two forms of imaging for PE: CT pulmonar y angiography (CTPA) and ventilation-perfusion (V/Q) scanning. CTPA uses a higher dose of r adiation (not good for young patients or pregnant patients), but will give a de \201 nitiv e answer, as well as diagnose other conditions often confused with PE (like aortic dissecti on). V/Q scanning uses a low dose of radiation (good for the young and pregnant), but may not gi ve a de \201 nitive answer. V/Q scans are reported as low, intermediate and high probabili ty of PE. The V/Q scan probability must concord with the clinical probability to diagnose o r exclude PE (both low probability or both high probability). All other combinations are no n-diagnostic and the patient must have a CTPA. Pitfalls in diagnosis \200 Investigating for PE because the patient has an elevated D-dim er. The D-dimer is irrelevant if there are no clinical symptoms or signs of PE. \200 Deci ding not to take the D-dimer because the patient is post-surgery, elderly, or has had recen t trauma. If the Wells score is <2.0, a D-dimer test is rapid and may avoid admission for d iagnostic imaging if normal. Treatment of pulmonary embolus Anticoagulate with LMWH and arrange to commence the patient on warfarin therapy. If the patient is ambulant, not hypoxic with a normal pulse rate and R R, many hospitals commence warfarin and follow-up as an outpatient. Admit patients who are hypoxic, hypotensive, tachycardic, tachypnoeic, or elderly for further management. Suspected massive PE \200 In patients with marked hypoxia and/or cardiovascular compromis e, call for urgent ICU expert help. If available, an emergency echo will demonstrate a dilated right ventricle and right heart failure. Do not take unstable patients for a CT or V/Q. \200 If suspicion of PE is high and the pa tient is haemodynamically unstable, administer thrombolytic therapy. Do not delay. Administ er alteplase (rTPA) 100mg over 2 hr or 0.6mg/kg (max 50mg) over 15min as per European Cardi ology guidelines ( www.escardio.org ). 122 CHAPTER 3 Medicine Upper gastrointestinal bleeding Causes of upper gastrointestinal bleeding Common \200 Pep tic ulceration. \200 Mucosal in \202 ammation (oesophagitis, gastritis, or duodenitis). \200 Oesophageal varices. \200 Mallory \200\223Weiss tear. \200 Gastric carcinoma. \200 Coagulation disorders (thrombocytopenia, warfarin). Rare \200 Aorto-enteric \201 stula (especially after aortic surgery). \200 Benign tumors (eg leiomyomas, carcinoid tum ors, angiomas). \200 Congenital (eg Ehlers \200\223Danlos, Osler \200\223Weber \200\223Re ndu, pseudoxanthoma elasticum). History Take a detailed history, whilst resuscitating as necessary. Upper GI bleeding usual ly presents with haematemesis and/or melaena. Major upper GI bleeding may present with fres h PR bleeding. Ask about the amount and duration of bleeding, any past history of GI bleeding or liver pro blems, and associated symptoms (abdominal pain, weight loss, anorexia). Syncope usually inf ers a signi \201 cant bleed. Take a full drug history (ask about aspirin, NSAIDs, warfarin , iron) and enquire about alcohol consumption. Examination Check ABCs. Rapidly assess for evidence of hypovolaemic shock (pulse and respir atory rates, BP, GCS, skin color/temperature, capillary re \201 ll). Look at any available vomit or feces. Check for abdominal masses, tenderness or surgical scars (including aortic grafting). Look for stigmata of liver disease. Perform a PR examination and check for feca l occult blood (FOB). Investigation and diagnosis Request old hospital notes and send blood for FBC, clotting scr een, U&E, blood glucose, Group and Save or cross-matching (according to clinical features). Urea may be i , but creatinine will be normal unless renal function is impaired. Check SpO 2 (obtain ABG if <94 % ) and consider CXR and ECG. Endoscopy is the investigation of choic e to identify the source of the bleeding. Risk of further bleeding and death The risk of mortality and further complications increase s with increasing age, co-morbidities (especially cancer and heart failure), liver disease, continued bleeding, elevated urea, and passage of PR blood. 123 UPPER GASTROINTESTINAL BLEEDING Table 3.7 Initial Rockall Score for risk of death in upper GI bleeding Points 0 1 2 3 Age <60 60 \200\22379 > 80 Shock HR<100 HR > 100 Systolic BP<100mmHg Systolic BP > 100mmHg Systolic BP > 100mmHg Renal failure Comorbidity Cardiac failure, ischaemic heart disease or any major co-morbidity Liver failure Disseminated malignancy Any score > 0 signi \201 es increased risk of mortality. Only consider patients scoring 0 on the initial Rockall score (Table 3.7 ), with no further evidence of bleeding, for discharge home from the ED with follow-up. Any patient scoring > 0 requires urgent endoscopy. Treatment of moderate/severe hemorrhage \200 Check airway and breathing. Provide O 2 to m aintain SpO 2 94 \200\22398 % . Insert 2 large (14G) IV cannulae, send FBC, U&E, clotting, cross-match. Start IV \202 uids followed by blood as necessary. \200 Avoid omeprazole acutely unless the patient has known peptic ulcer disease (give 40mg diluted in 100mL saline as IVI over 30min). If the patient is anticoagulated, or has a clotting disorder (eg due to liver disease), dis cuss with a hematologist and give vitamin K/clotting factors/fresh frozen plasma (FFP) acco rdingly. Insert a urinary catheter and monitor the urine output. \200 Ensure that patients with se vere uncontrolled variceal bleeding, severe encephalopathy, hypoxia, acute agitation, or ev idence of aspiration have their airways secured, if necessary by tracheal intubation. Managing severe hemorrhage possibly due to varices For unstable patients with a past histor y of varices or clinical features of hepatic failure, arrange emergency endoscopic treatmen t: \200 Commence \202 uid rescucitation. \200 Give terlipressin (2mg IV repeated ever y 4 \200\2236hr). \200 Check International Normalized Ratio (INR) and give IV vitamin K i f prolonged. Give prophylactic antibiotics eg cipro \202 oxacin or second/third generation cephalosporin which may d mortality in severe hemorrhage. Consider ballon tamponade as a salvage procedure in a patient with massive hemorrhage, at r isk of death. If experienced in the technique, insert a 4 lumen Sengstaken/Minnesota tube. In \202 ate the gastric balloon then the oesophageal balloon to a pressure of 30 \200\2234 0mmHg in order to tamponade the bleeding varices. Regularly aspirate both ports. See http://www.sign.ac.uk 124 CHAPTER 3 Medicine Lower gastrointestinal bleeding The commonest cause of apparent lower GI bleeding is upper GI haem- orrhage. 820 % of acute GI hemorrhage is from the colon or rectum. Angiodysplasia and bleeding from diverticulae are the most frequent causes, but in \202 ammatory bowel di sease or, very rarely, aorto-enteric \201 stulae may be responsible. Lower GI hemorrhage often settles spontaneously: localization of the bleeding source may be dif \201 cult. History Nature of bleeding Melaena may occur following small bowel or proximal colon bleedi ng, as well as upper GI hemorrhage. Conversely, large volumes of fresh or \200\230plum-col ored \200\231 rectal bleeding may follow upper GI hemorrhage. Bloody diarrhea suggests in \202 ammatory bowel disease or infective colitis. Associated symptoms Weight loss, anorexia, or a change in bowel habit raise suspicion of co lonic carcinoma. Abdominal pain may be a feature of ischaemic colitis, in \202 ammatory bo wel disease, or carcinoma. Anal pain commonly occurs with anal \201 ssure or complication of hemorrhoids. Syncope or postural dizziness May indicate signi \201 cant hemorrhage. Past medical history Ask about in \202 ammatory bowel disease, peptic ulceration, or other illnesses. Previous aortic surgery with graft insertion can rarely result in formation of an aorto-enteric \201 stula (symptoms include sporadic or fulminant bleeding, often with syncope). Drug history Ask about salicylates, NSAIDs, corticosteroids, and anticoagulants. Family and social history Note any family history of peptic ulcers, in \202 ammatory bowel disease. Enquire about alcohol consumption. Examination First assess for signs of hypovolaemia and commence resuscitation if nec- essar y. Document pulse, BP (comparing erect and supine, noting any pos- tural drop), T and Sp O 2 . Examine the abdomen and PR in all cases. Investigations Obtain blood for cross-matching (ask for 4 \200\2236U of type speci \201 c if urgent), FBC, U&E, glucose, and coagulation studies. Perform an ECG on any patient > 50 years. Risk of further bleeding and death The risk of mortality and further complications increase s with increasing age, co-morbidities, haemodynamic disturbance, and the use of NSAIDs or a spirin. Only consider discharge if the patient is young, otherwise healthy, has passed only a small amount of blood PR, and does not take NSAIDs or anticoagulants. Always arrange fol low up for these patients. 125 LOWER GASTROINTESTINAL BLEEDING Treatment Patients with signs of hypovolaemia require immediate resuscitation: \200 Give O 2 . \200 Attach monitoring (cardiac monitor, S pO 2 , BP monitoring). \200 Insert two large bore IV cannulae. \200 Give 1L of 0.9 % saline or Hartmann \200\231s solution IV s tat and give further \202 uids according to response. Insert a NG tube. \200 Insert a urinary catheter. \200 Correct any coagulopathy. \200 Consider the need for a central venous line. \200 Contact the surgical team and ICU. See http://www.sign.ac.uk 126 CHAPTER 3 Medicine Headache Headaches of non-traumatic origin account for 8 0.5 % of ED attendances; 10 \200 \22315 % have serious underlying pathology. Patients typically present in one of three ways : \200 Severe headache, unlike any previous one ( \200\230 \201 rst severe \200\231 or \200\230worst ever \200\231). Headache with associated worrying features (altered mental status, fever, focal neurology). Chronic severe headache unresponsive to treatment. Causes Primary headaches \200 Migraine. \200 Tension headaches. \200 Cluster headache s. \200 Miscellaneous (benign cough headache, benign exertional headache, headache associated with sexual activity). Secondary headaches \200 Head injury. \200 Vascular (stroke, intracranial haematoma, su barachnoid hemorrhage, unruptured arterio-venous malformation, venous thrombosis, hyper- te nsion). Non-vascular intracranial disorder ( i cerebrospinal \202 uid (CSF) pres- sure, post-LP, intracranial tumor). Substance misuse or withdrawal (including analgesia withdrawal or rebound). Infection (encephalitis or meningitis). \200 Metabolic (hypoxia, hypercapnoea, hypoglycae mia, carbon monoxide (CO) poisoning, dialysis). Craniofacial disorder (pathology of skull, neck, eyes, nose, ears, sinuses, teeth, mouth, temporomandibular joint dysfunction). \200 Neuralgias (trigeminal, occipita l and other cranial nerves). Approach Use a detailed history and examination (including vital signs and neurolog- ical e xamination) to search for potentially serious causes. Look particularly for the following ( some typical features in brackets): \200 Subarachnoid hemorrhage (sudden, severe onset, syncope) \200\224 b p.128. Meningitis or encephalitis (fever, neck rigidity) \200\224 b p.224. \200 Head injury (hi story or signs of trauma) \200\224 b p.354. \200 i intracranial pressure (papilloedema, loss of retinal vein pulsation). \200 Stroke (focal neurological signs) \200\224 b p.144 . \200 Acute glaucoma (painful red eye, d VA, irregular semi-dilated pupil) \200\224 b p.542. Cranial arteritis (jaw pain, temporal artery tenderness) \200\224 b p.132. 127 HEADACHE History Features suggesting possible serious pathology are: \200 Sudden onset headache. \200 Worst headache ever. \200 Dramatic change in pattern of headache. \200 Known HIV or malignancy. \200 The presence of a ventriculo-peritoneal shunt. \200 Headache coming on during exertion. \200 New onset headache in those aged > 50 years. Ask about drugs an d the possibility of toxins (eg CO). Examination Check GCS, pulse rate, respiratory rate, BP, T and SpO 2 : \200 Feel the h ead for muscular tenderness, arterial tenderness, trigger points for neuralgia, and look for evidence of head injury. Examine the eyes for VA, pupil reactions, eye movements. Look at the fundi for papilloedema. Palpate the sinuses for tenderness. \200 Look in the ears for haemotympanum or infection. \200 Check the oral cavity for infection. \200 Look for evidence of purpura/rash of me ningococcal infection. \200 Complete a full neurological examination (include cranial ner ves, limb tone, power, sensation, co-ordination and re \202 exes). Check for Kernig \200\231s sign : straightening the knee whilst the hip is \202 exed prod uces discomfort in the presence of meningeal irritation. Management Investigation and emergency treatment will be tailored according to the presenta tion of the patient, based upon the likely diagnosis. \200 Check FBC, ESR, CRP, U&E, bloo d glucose. \200 If pyrexial and no other obvious source of infection found, take blood cultures and consider IV cefotaxime 2g. Start IV \202 uids and admit. Give paracetamol (oral or IV if vomiting) and an NSAID. \200 An effective treatment for h eadache is IV metoclopramide 10mg with IV \202 uids. Arrange an emergency CT brain for any patient with an acute severe headache, or with a hist ory of seizure, or an abnormal neurological exam. Arrange a CT for any patient with HIV. If subarachnoid hemorrhage is suspected and CT normal, admit for lumbar puncture. It may be safe to discharge home a patient with slow onset headache that has resolved follo wing treatment, with normal examination and blood tests. Arrange GP follow up. Always advis e to reattend if symptoms worsen. 128 CHAPTER 3 Medicine Subarachnoid hemorrhage Consider subarachnoid hemorrhage in any \200\230worst ever \200\231 or sudden onset headac he Atraumatic subarachnoid hemorrhage can occur at any age and is an important cause of sud den collapse and death. Most bleeds follow rupture of saccular ( \200\230berry \200\231) an eurysms in the circle of Willis. Other bleeds may be due to arteriovenous malformations, tu mors, or connective tissue disorders. History Up to 70 % of patients with subarachnoid hemorrhage report rapid onset or \200\230 worst ever \200\231 headache. This is classically described as \200\230like a blow to the back of the head \200\231, accompanied by neck pain, photophobia, and vomiting. In 25 % , e xertional activities precede the event. The patient may present after syncope or \201 ts. Drowsiness and confusion are common. \200\230Warning headaches \200\231 may precede subar achnoid hemorrhage. Unilateral eye pain may occur. Examination Document pulse rate, BP, T o , and GCS. An unconscious patient with signs of Cu shing \200\231s response signi \201 es i intracranial pressure. Perform full cranial and p eripheral nerve examination. There may be focal motor and sensory signs due to intracerebra l extension of the hemorrhage or vasospasm, subhyaloid hemorrhages (blotchy hemorrhages see n in the fundi) or cranial nerve palsies. Oculomotor nerve palsy is characteristic of a ber ry aneurysm involving the posterior communicating artery. Neck stiffness is often absent in ED presentations, either because meningeal irritation has not yet occurred or because the patient is deeply unconscious. Investigation This may need to proceed alongside resuscitation in seriously ill patients: \200 Assess airway and breathing. If the patient is unconscious, open the airway and conta ct ICU. Consider urgent RSI, tracheal intubation and ventilation. Obtain venous access and check BMG, FBC, clotting screen, U&E. \200 CXR may show changes of neurogenic pulmonary oedema. \200 ECG may demonstrate ischaemic changes. \200 Arrang e emergency CT scan for all suspected cases (maximally sensitive within 12hr). Admit for lu mbar puncture (LP) (done > 12hr after head- ache onset) even if CT scan is normal. Involve the neurosurgical team early. It may be useful to use the Hunt and Hess score (see Table 3.8 ) when communicating severity by phone. 129 SUBARACHNOID hemorrhage Table 3.8 Hunt and Hess scale for subarachnoid haemorrahage Grade 1 Asymptomatic, mild headache, slight nuchal rigidity 2 Moderate to severe headache, nuchal rigidity, no neurologic de \201 cit other than cranial nerve palsy 3 Drowsiness/confusion, mild focal neurological de \201 cit 4 Stupor, moderate-severe hemiparesis 5 Coma, decerebrate posturing Treatment Tailor this according to the presentation and the need for resuscitation: \200 Maintain SpO 2 94 \200\22398 % . \200 Provide adequate analgesia and antiemetic. Codeine (30 \200\22360mg PO), paracetamol (1g PO) and/or NSAID may suf \201 ce. Some patients requ ire more potent analgesics (eg morphine titrated in 1mg increments IV according to response ) \200\224 proceed slowly to avoid drowsiness. If unconscious (GCS < 8), severely agitated or combative, tracheal intu- bation (with gener al anesthetic (GA)) will allow IPPV and control of pCO 2 to within normal levels. Insert a urinary catheter and arterial line. Contact neurosurgical team \200\224 further treatment options include: \200 Nimodipine ( 60mg PO every 4hr or 1mg/hr IVI) to prevent and treat ischaemic neurological de \201 cits secondary to vasospasm. \200 Mannitol IV (eg 200mL o f 10 % ) if there is evidence of i ICP. 130 CHAPTER 3 Medicine Migraine Patients with recurrent migraine rarely attend the ED unless symptoms are differen t from usual \200\224 take care to avoid missing more serious condi- tions. The pathogenes is of migraine is not entirely clear, but there is initial vasoconstriction and subsequent vasodilatation of both intracranial and extracranial blood vessels. Presentation Precipitants include fatigue, alcohol, menstruation, oral contraceptive pill ( OCP), hunger, chocolate, cheese, shell \201 sh, and red wine. A prodrome lasting 5 \200\22330min occurs in a third of patients, with blurred vision, phot ophobia, or scintillating scotomata (an area of blurred or absent vision surrounded by movi ng zig-zag lines), malaise, anorexia, and vomiting. A few experience hemiparaesthesiae, mil d unilateral weakness, ataxia, or dysphasia. The following headache may last 4 \200\22372hr , and is usually \200\230throbbing \200\231 and unilateral, but may be generalized. Photop hobia, nausea, or phonophobia is common. Rare forms of migraine Hemiplegic migraine Profound hemiplegia precedes the development of the headache by 30 \200\22360min. The weakness and other focal de \201 cits usually resolv e quickly. Occasionally, they may be slow or fail to resolve. Basilar migraine Brainstem disturbances, with impaired consciousness, vertigo, dysarthria, diplopia, and limb weakness. Ophthalmoplegic migraine Transient unilateral ophthalmoplegia and ptosis, which may last se veral days. Acephalgic migraine Very occasionally, neurological defects may be present without headache . Examination Look for evidence of other serious diagnoses. Treatment of acute attacks \200 Give simple analgesia (eg paracetamol 1g PO PRN qds or NS AID) in combination with an anti-emetic (eg metoclopramide 10mg PO, or IV). \200 Refer fo r admission patients who have neurological signs, altered mental status, or where there is diagnostic uncertainty (including change in severe headache pattern). Acute attacks that fail to respond to simple measures may respond to other drugs, but these are associated with signi \201 cant adverse effects. 5HT 1 agonist sumatriptan (6mg SC or 50mg PO or 20mg intranasally) is effective, but discuss with a senior \201 rst. Sumatriptan causes vasoconstriction and is therefore contraindicated in IHD, uncontrolled h ypertension, basilar, and hemiplegic migraine. Rebound headache may occur in up to 45 % .