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Emergency Medicine > Gastrointestinal emergencies > Flashcards

Gastrointestinal emergencies Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

Cardiovascular causes of the acute abdomen?

A
  • Acute coronary syndrome
  • Acute mesenteric ischaemia
  • Ruptured AAA
  • Aortic dissection
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2
Q

Gastrointestinal causes of the acute abdomen?

A
  • GI tract perforation
  • Mechanical bowel obstruction
  • Acute appendicitis
  • Peptic ulcer disease
  • Diverticulitis
  • Constipation
    *
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3
Q

Biliary and pancreatic causes of the acute abdomen?

A
  • Acute pancreatitis
  • Gallstones
  • Acute cholecystitis
  • Ascending cholangitis
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4
Q

Genitourinary causes of the acute abdomen?

A
  • Ruptured ectopic pregnancy
  • Ovarian torsion
  • Testicular torsion
  • Acute pyelonephritis
  • Kidney stones
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5
Q

Presentation of ruptured AAA?

A
  • Sudden, severe chest/abdominal pain, radiates to the back
  • Hypotension/shock
  • Pulsatile mass in abdomen
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6
Q

Diagnosis of ruptured AAA?

A
  • If the patient is unstable, diagnosis should not delay management.
  • If the patient is hemodynamically stable, abdominal ultrasound can confirm diagnosis.
  • CT/MR angiography can be used to localise rupture site and plan surgical management.
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7
Q

Presentation of oesophageal rupture?

A
  • Mackler’s triad:
    • Vomiting and/or retching
    • Severe retrosternal pain that radiates to the back
    • Subcutaneous/mediastinal emphysema
      • Crackling sound when auscultating mediastinal region (Hamann sign)
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8
Q

What is Boerhaave syndrome?

A
  • Transmural oesophageal rupture secondary to severe vomiting/coughing
  • Risk factors include chronic cough, alcoholism, repeated episodes of vomiting
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9
Q

Diagnosis of oesophageal rupture?

A
  • Chest x-ray
    • Widened mediastinum
    • Pneumomediastinum
    • Pleural effusion
  • CT scan
    • Same findings as CXR
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10
Q

What is shown on this x-ray?

A
  • Pneumomediastinum (shown in green)
  • This patient has Boerhaave syndrome (oesophageal rupture)
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11
Q

Management of oesophageal rupture?

A
  • ABCDE approach
  • Nil-by-mouth
  • Broad-spectrum IV antibiotic prophylaxis
  • Non-surgical (expectant) management:
    • Small, contained perforation
  • Surgical management:
    • Haemodynamic instability or larger perforation
    • Surgical closure of the rupture
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12
Q

Complications of peptic ulcer disease?

A
  • Gastrointestinal bleeding
    • Gastric ulcers of the lesser curvature may cause bleeding from the left gastric artery
    • Posterior duodenal arteries may cause bleeding from the gastroduodenal artery
  • Perforation
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13
Q

Presentation of a perforated peptic ulcer?

A
  • Sudden, diffuse abdominal pain
  • Peritonism (guarding and rebound/percussion tenderness)
  • Fever, tachycardia, hypotension
  • Shoulder-tip pain (irritation of the phrenic nerve)
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14
Q

Diagnosis of a perforated peptic ulcer?

A
  • Upright chest x-ray
    • 75% will have free air under the diaphragm
  • Diagnosis is usually clinical
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15
Q

Management of a perforated peptic ulcer?

A
  • ABCDE
  • Fluid resuscitation
  • Nil-by-mouth
  • Surgical repair using a patch of omentum
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16
Q

Presentation of GI perforation?

A
  • Sudden-onset diffuse abdominal pain
  • Constipation/obstipation
  • Nausea/vomiting
  • Peritonism
    • Guarding, rebound tenderness
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17
Q

Diagnosis of GI perforation?

A
  • Chest x-ray:
    • Free air under the diaphragm
    • Patient must be sat upright
    • Can be done quickly in A&E, with much lower radiation dose than an abdominal x-ray
  • Abdominal x-ray:
    • Pneumoperitoneum
  • CT with contrast
    • Most sensitive investigation
    • Shows pneumoperitoneum
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18
Q

What does this x-ray show?

A

Pneumoperitoneum (shown in green)

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19
Q

Management of GI perforation?

A
  • Supportive care
    • Stable patient
    • IV PPI
    • Opioid analgesics (unless also bowel obstruction)
    • Antiemetics
  • Surgical management
    • Most patients require an urgent exploratory laparotomy
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20
Q

Commonest causes of small bowel obstruction?

A
  • Bowel adhesions
    • Commonest cause
    • History of GI surgery
  • Incarcerated hernias
    • Second commonest cause
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21
Q

Commonest causes of large bowel obstruction?

A
  • Malignancy
    • Commonest cause of LBO
  • Diverticulitis
  • Volvulus
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22
Q

Presentation of mechanical bowel obstruction?

A
  • Colicky abdominal pain
  • Obstipation
  • Abdominal distension
  • Progressive nausea and (bilious) vomiting
  • Tinkling bowel sounds
  • History of abdominal surgery
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23
Q

Diagnosis of mechanical bowel obstruction?

A
  • Abdominal x-ray
    • Distended loops of bowel proximal to the obstruction
    • Air-fluid levels
  • CT abdomen with contrast
    • Similar findings
    • Transition point at site of obstruction
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24
Q

How to differentiate between SBO and LBO?

A
  • The folds in the bowel on AXR
    • Small bowel folds (valvulae conniventes) = visible across the whole width of the bowel
    • Large bowel folds (haustra) = don’t completely transverse the bowel
    • Rule of thumb - haustra can sometimes appear to cross the full width of the large bowel.
  • The anatomical position of the distended bowel loops
  • The history
    • SBO = early vomiting, late obstipation
    • LBO = early obstipation, late vomiting
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25
Q

What is the 3/6/9 rule?

A
  • Upper limits of normal for the diameter of bowel segments are as follows:
    • Small bowel = 3cm
    • Large bowel = 6cm
    • Caecum = 9cm
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26
Q

Management of mechanical bowel obstruction?

A
  • Nil-by-mouth
  • “Drip and suck”
    • IV fluids
    • Nasogastric tube decompression
  • Most will require surgical management
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27
Q

Causes of paralytic ileus (functional bowel obstruction)

A
  • Intraabdominal surgery
  • Intraabdominal infection/inflammation
  • Medications (e.g. anticholinergics, opioids)
  • Hypokalaemia
  • Sepsis

The 5 P’s: Peritonitis, Postoperative, low Potassium, Painkillers (opioids), Pelvic/spinal fractures are some of the common causes

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28
Q

Presentation of paralytic ileus?

A
  • Constipation and reduced flatulence
  • Continuous (non-colicky) abdominal pain
  • Abdominal distention
  • Nausea and vomiting
  • Decreased or absent bowel sounds
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29
Q

Diagnosis of paralytic ileus?

A
  • CT abdomen
    • Gold standard
    • Diffuse small and/or large bowel distention
  • Abdominal x-ray
    • Less sensitive than CT
    • Same findings as CT
  • Abdominal ultrasound
    • Not routinely used in adults, but is the investigation of choice in children
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30
Q

Management of paralytic ileus?

A
  • Nil-by-mouth
  • “Drip and suck”
    • IV fluids
    • NG tube decompression
  • Correct underlying cause if possible
  • Avoid opiate analgesia
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31
Q

Presentation of acute appendicitis?

A
  • Abdominal pain
    • Initially central/diffuse
    • Eventually localises to RIF
  • Fever
  • Tachycardia
  • Nausea/anorexia

Examination

  • Rosving’s sign - palpation of LIF causes RIF pain
  • Psoas sign - extension of right leg (in L lateral position) causes RIF pain
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32
Q

Diagnosis of acute appendicitis?

A
  • FBC
    • Neutrophilic leukocytosis
  • Abdominal ultrasound
    • Distended, aperistaltic appendix
  • Abdominal CT scan
    • Periappendiceal fat stranding
    • Distended appendix
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33
Q

Management of acute appendicitis?

A
  • Laparoscopic appendicectomy
  • Prophylactic IV antibiotics
  • If the appendix has perforated then patients will need a peritoneal lavage
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34
Q

Causes of intussusception?

A
  • No identifiable cause in 75%
  • Meckel’s diverticulum (commonest cause found in children)
  • Polyps/malignancy (commonest cause found in adults)
  • Enlarged Peyer’s patches
    • Lymphoid patches on the wall of the ileum
    • Can become hypertrophied after infection/vaccination
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35
Q

Presentation of intussusception?

A
  • Acute colicky abdominal pain
  • Infants often draw legs up during episodes
  • Sausage-shaped RUQ mass
  • Vomiting
  • “Redcurrant jelly” stools (due to PR bleeding)
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36
Q

Diagnosis of intussusception?

A
  • Abdominal ultrasound (best initial investigation)
    • Target sign - telescoping section of bowel appears as rings on a target
  • Contrast enema with ultrasound/fluoroscopy (best confirmatory test)
  • Abdominal CT
    • Used if the diagnosis is equivocal after ultrasound and AXR
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37
Q

Management of intussusception?

A
  • NGT decompression and fluid resuscitation if needed
  • Non-surgical
    • Air enema is the treatment of choice
  • Surgical management
    • Indicated if the patient is unstable (e.g. perforation) or if a pathological lead point is suspected (e.g. malignancy)
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38
Q

Presentation of acute mesenteric ischaemia?

A
  • Age > 60, VTE risk factors (usually have AF).
  • Severe pain out of proportion to examination findings (often normal BP, HR etc.)
  • Diffuse abdo pain and distension
  • Nausea and vomiting
39
Q

Diagnosis of acute mesenteric ischaemia?

A
  • Lactic acidosis
  • Abdominal x-ray: normal early on, progressing to pneumatosis (gas in the walls of the intestines).
  • CT angiography gold standard
40
Q

Management of acute mesenteric ischaemia?

A
  • ABCDE
  • NGT decompression
  • IV fluid resuscitation
  • Prophylactic IV antibiotics
  • Emergency laparotomy and resection of necrotic bowel preferred in most
  • If the patient is stable revascularization may be attempted
  • Optimise AF treatment if appropriate to reduce the risk of recurrence
41
Q

Types of volvulus and malrotation?

A
  • Sigmoid colon - commoner in the elderly
  • Caecal volvulus - commoner in 40-60 year-olds
  • Midgut volvulus and malrotation - commoner in children
42
Q

Presentation of volvulus?

A
  • Abdominal pain
    • Episodic
    • Relieved by the explosive passage of stool/gas
  • Distension
  • Vomiting & constipation
  • Peritonitis if the bowel perforates
43
Q

Diagnosis of volvulus?

A
  • Abdominal x-ray
    • Sigmoid volvulus: large bowel obstruction with ‘coffee bean sign’
    • Caecal volvulus: small bowel obstruction
44
Q

What is shown on this x-ray?

A

Sigmoid volvulus with the coffee bean sign

45
Q

Management of volvulus?

A
  • Sigmoid volvulus
    • Rigid/flexible endoscopic decompression, detorsion, and reduction
    • Surgery if bowel perforates
  • Caecal volvulus
    • Typically requires surgical management
    • Right hemicolectomy is often needed
46
Q

What is acute megacolon?

A
  • Imbalance in parasympathetic and sympathetic nervous system → progressive abdominal distention
  • Often occurs in seriously ill patients who have undergone major surgery
47
Q

Management of acute megacolon?

A
  • Supportive measures
    • NGT decompression
    • Nil-by-mouth
    • IV fluids
  • Neostigmine
  • Surgery
    • Indicated if conservative measures fail
48
Q

What is toxic megacolon?

A
  • A form of megacolon occurring as a result of infective/inflammatory colitis
  • Commonly secondary to C. difficile infection
  • May also occur secondary to IBD
49
Q

Presentation of toxic megacolon?

A
  • Bloody diarrhoea
  • Vomiting
  • Abdominal distention and pain
  • Signs of sepsis
50
Q

Diagnosis of toxic megacolon?

A
  • Abdominal x-ray
    • Dilated colon
    • Loss of haustration
    • Multiple air-fluid levels
51
Q

Management of toxic megacolon?

A
  • Supportive care
    • Will likely need escalating to HDU/ICU
    • Nil-by-mouth
    • NGT
    • IV fluid
  • Surgery
    • If no improvement within 24-72 hours or the development of complications
52
Q

Presentation of a strangulated abdominal hernia?

A
  • Acute abdominal pain localising to the site of the hernia
  • Features of bowel obstruction (if bowel is part of hernial contents)
  • Tender, irreducible hernia
  • Toxic appearance, fever, signs of sepsis
53
Q

Management of a strangulated abdominal hernia?

A
  • ABCDE and resuscitation
  • Surgical hernia repair
  • Do not attempt manual reduction as this can cause generalised peritonitis
54
Q

Presentation of acute cholecystitis?

A
  • Right upper quadrant pain
    • Typically more severe and prolonged (> 6hrs) than biliary colic
  • Positive Murphy’s sign
    • Sudden pausing during inspiration on deep palpation of the RUQ due to pain.
  • Fever, anorexia
  • Guarding
55
Q

Diagnosis of acute cholecystitis?

A
  • Blood tests to support clinical diagnosis
    • Raised WCC and CRP
    • LFTs - transaminitis
  • RUQ ultrasound scan if the diagnosis is uncertain
    • Shows gallbladder wall thickening
56
Q

Management of acute cholecystitis?

A
  • Elective laparoscopic cholecystectomy (within 1 week)
  • Prophylactic IV antibiotics
57
Q

Pathophysiology of acute cholecystitis?

A
  • Biliary tract obstruction → bile stasis → ascending bacterial infection
  • May be iatrogenic through the introduction of GI contents into bile ducts e.g. ERCP, biliary stenting, or liver transplantation
58
Q

Presentation of ascending cholangitis?

A
  • Charcot’s triad (present in up to 70%)
    • RUQ pain
    • Jaundice
    • Fever
  • Reynold’s pentad
    • Charcot’s triad
    • Mental status changes
    • Hypotension
59
Q

Diagnosis of ascending cholangitis?

A
  • Laboratory tests to confirm clinical diagnosis
    • FBC → raised WCC
    • CRP → raised
    • LFT → cholestasis (raised ALP, bilirubin, GGT, ALT)
  • RUQ ultrasound scan if diagnosis is uncertain
    • Shows dilated common bile duct
60
Q

Management of ascending cholangitis?

A
  • IV antibiotics
  • ERCP after 24-48 hrs to relieve any obstruction
61
Q

Risk factors for spontaneous bacterial peritonitis?

A
  • Liver disease and ascites
  • Upper GI bleeding
  • Previous SBP
62
Q

Presentation of spontaneous bacterial peritonitis?

A
  • Diffuse abdominal pain and tenderness
  • Fever and rigors
  • Worsening ascites
  • New-onset or worsening encephalopathy
63
Q

Diagnosis of spontaneous bacterial peritonitis?

A
  • Paracentesis and M, C & S of ascitic fluid
  • Commonest organism found is E. coli
64
Q

Management of spontaneous bacterial peritonitis?

A
  • IV antibiotics (usually cefotaxime)
  • Antibiotic prophylaxis is given if a patient with ascites:
    • Has had a previous episode of SBP
    • Has fluid protein < 15g/L
65
Q

Causes of acute pancreatitis?

A

I GET SMASHED

  • I - iatrogenic
  • G - gallstones
  • E - ethanol (alcohol intoxication)
  • T - trauma
  • S - steroids
  • M - mumps
  • A - autoimmune
  • S - scorpion venom
  • H - hyperlipidaemia, hypercalcaemia
  • E - ERCP
  • D - drugs (e.g. azathioprine, loop diuretics, anticonvulsants)
66
Q

Clinical features of acute pancreatitis?

A
  • Constant, severe epigastric pain
    • Classically radiates to the back
  • Nausea, vomiting
  • Fever
  • Signs of shock: hypotension, tachycardia, oliguria/anuria
  • Cullen’s sign - periumbilical bruising
  • Gray-Turner’s sign - flank bruising
67
Q

Diagnosis of acute pancreatitis?

A
  • Early ultrasound scan important to assess whether gallstones are involved as this affects management
  • Serum markers to aid clinical diagnosis
    • Serum amylase raised in 75% of patients
    • Serum lipase - longer half-life so may be useful for later presentation
68
Q

What scoring system is used to assess severity?

A

Glasgow score

69
Q

Management of acute pancreatitis?

A
  • Aggressive fluid resuscitation
  • Analgesia - IV opioids
  • Don’t need to be nil-by-mouth unless they are vomiting
  • Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy
  • Patients with biliary obstruction should undergo early ERCP
70
Q

What scoring system is used to assess acute upper GI bleeding?

A

The Glasgow-Blatchford scale. Variables included are:

  • Urea
  • Haemoglobin
  • Systolic BP
  • The presence of:
    • Syncope
    • Malaena
    • Tachycardia
    • Hepatic failure
    • Cardiac failure

A score of 0 indicates a patient can be considered for early discharge

71
Q

Resuscitation of a patient with an acute upper GI bleed?

A
  • ABCDE
  • Wide-bore IV access (e.g. 2 x grey cannulas)
  • Platelet transfusion
    • Actively bleeding and platelets < 50 x 109
  • Fresh frozen plasma
    • Fibrinogen < 1g/L
    • APTT or PT > 1.5 x normal
  • Prothrombin complex concentrate
    • Taking warfarin and bleeding
72
Q

Investigation of patients with acute upper GI bleeding?

A
  • Upper GI endoscopy
    • Should be offered immediately after resuscitation if severe bleeding
    • All patients should have endoscopy within 24 hours
73
Q

Management of variceal bleeding?

A
  • Terlipressin and prophylactic antibiotics should be given at presentation
    • Before endoscopy if known history of varices
  • Elastic band ligation of oesophageal varices is first line
  • If vessels can’t be visualised (too much blood) or elastic band ligation fails to control bleeding, a Sengstaken-Blakemore tube can be inserted
    • Expands against the walls of the oesophagus and physically tamponades the vessels
    • Mustn’t be left in longer than 2 days as can cause oesophageal necrosis
  • Definitive management of varices is a transjugular intrahepatic portosystemic shunt (TIPS) procedure that relieves backpressure in the portal vein.
74
Q

Management of non-variceal bleeding?

A
  • Endoscopy to look for cause
  • IV PPIs
    • Only given after endoscopy if confirmed non-variceal bleed
75
Q

Priorities in assessment and management of a lower GI bleed?

A
  1. Consider (and exclude by urgent endoscopy) an upper GI source of bleeding
  2. Urgent involvement of surgical teams if there is major blood loss and/or haemodynamic instability
  3. Consider and correct clotting abnormalities
    • Consider reversing anticoagulation
  4. Blood transfusion
    • Transfuse when Hb < 80g/L if bleeding has stopped
    • Threshold is Hb < 100g/L if ongoing bleeding
  5. Admit or discharge?
    • Minor lower GI bleeding that stops spontaneously → early outpatient sigmoidoscopy
    • Admit if moderate/severe bleeding or significant comorbidities
76
Q

Investigation of a suspected acute flare-up of IBD?

A
  • Abdominal x-ray to rule-out toxic dilatation (megacolon) or proximal constipation
  • Blood tests:
    • FBC
    • CRP (raised in 90%)
      • In patients with normal CRP platelets can be a marker of disease severity
    • U&Es
      • Dehydration indicates late presentation and a severe flare
    • Stool sample
      • Infection can trigger flares
      • Rule-out C. difficile → pseudomembranous colitis
77
Q

Management of an acute flare-up of ulcerative colitis?

A
  • Drug therapy
    • Oral prednisolone (poorly absorbed in severe flare → IV hydrocortisone)
    • Ciclosporin/infliximab if poor response to steroids
  • Surgery
    • If medical management fails
    • Crohn’s disease must be definitively ruled-out
    • Colectomy/hemicolectomy depending on how diffuse the illness is
78
Q

Management of an acute flare-up of Crohn’s disease?

A
  • Drug management
    • Glucocorticoids (PO or IV) are first-line to induce remission
    • Azathioprine or mercaptopurine may be used second-line
      • TPMT levels must be measured before starting these
    • Methotrexate is an alternative second-line drug
    • Infliximab can be used in refractory cases
  • Surgical management
    • Reserved for when medical management fails
    • Recurrence within one year in 80% of cases
    • Aims to remove as little of the gut as possible
    • May end up with a short gut/ileostomy
79
Q

Causes of acute liver failure?

A
  • Hepatotoxic substances
    • Drugs: paracetamol
    • Alcohol
    • Cocaine (causes vasoconstriction → hepatic hypoperfusion)
  • Infections
    • Hepatitis A, B, E (or superinfection with B & D)
  • Vascular
    • Budd-Chiari syndrome (hepatic vein thrombosis)
  • Pregnancy-related
    • HELLP syndrome, acute fatty liver of pregnancy
  • Autoimmune hepatitis
80
Q

Clinical features of acute liver failure?

A
  • Hepatic encephalopathy
    • Altered consciousness
    • Asterixis
  • Jaundice
  • Pruritis
  • Abdominal pain
  • Nausea and vomiting
  • Anorexia
81
Q

Definition of acute liver failure?

A

ALF is defined as:

  • Severe acute liver injury
  • Encephalopathy
  • Impaired liver synthetic function (prothrombin time/international normalized ratio 1.5)
  • In the absence of pre-existing liver disease
82
Q

Investigation of suspected acute liver failure?

A
  1. Detailed drug history (including any herbal and over-the-counter medications) from the patient or family members
    • If ALF is suspected to be due to paracetamol poisoning start NAC without delay
  2. Arrange urgent investigations:
    • PT, APTT, INR
    • FBC
    • Blood glucose
    • U&Es - ?hepatorenal syndrome
    • LFT
    • ABG if reduced consciousness
    • Culture and microscopy of ascitic fluid
    • Liver ultrasound
83
Q

Management of acute liver failure

A
  • Seek hepatology advice
  • Escalate to HDU (or ITU if encephalopathy is severe)
  • Manage complications (e.g. AKI, sepsis, SBP)
  • Liver transplantation
    • Indications vary depending on pathology
    • Generally require deranged INR (> 6.5)
84
Q

What is decompensated liver disease?

A
  • Background of chronic liver disease
  • Acute hepatic decompensation → liver failure
    • Jaundice
    • Prolongation of the prothrombin time/international normalized ratio
  • Extrahepatic organ failure
85
Q

Management of decompensated chronic liver disease?

A
  1. Fluid and electrolyte balance
  2. Thromboprophylaxis - LMWH
    • Increased risk of thromboembolism despite prolonged PT/APTT
  3. Drugs
    • IV vitamin K & oral folic acid once daily
    • Avoid opioids and sedatives
  4. Nutritional support
86
Q

What is hepatorenal syndrome?

A
  • AKI in the context of acute, severe liver failure when other causes of AKI have been excluded
  • Low albumin → low oncotic pressure → ascites → hypovolemia → renal hypoperfusion → activation of RAA system → renal artery constriction → further renal hypoperfusion and AKI
87
Q

LFT results in alcoholic hepatitis?

A
  • Gamma-GT characteristically raised (Gin and Tonic → gGT raised in ALD)
  • Transaminitis
    • AST:ALT normally > 2, ratio > 3 → suggests severe alcoholic hepatitis
88
Q

Management of alcoholic hepatitis?

A
  • Supportive care (e.g. nutritional support, fluid balance etc.)
  • Glucocorticoids is sometimes beneficial
    • “Discriminant function” is a score used to determine this
    • Calculation involves PT and bilirubin levels
    • Improves symptoms but increases the risk of infection and doesn’t improve prognosis
  • Pentoxyphylline sometime used
89
Q

Clinical features of hepatic encephalopathy?

A
  • Confusion, altered GCS
  • Asterixis - “liver flap”
  • Apraxia (e.g. can’t draw a 5-pointed star)
  • Likely jaundiced
90
Q

Investigation and diagnosis of hepatic encephalopathy?

A
  • Investigations
    • Check for infection (e.g. FBC)
    • Abdominal x-ray (?constipation)
    • PR examination & stool sample (?GI bleed)
    • EEG
  • Diagnosis
    • Usually clinical diagnosis, investigations help identify precipitating factor
91
Q

Grading of hepatic encephalopathy?

A
  1. Irritability
  2. Confusion, inappropriate behaviour
  3. Incoherent, restless
  4. Coma
92
Q

Management of hepatic encephalopathy?

A
  • Lactulose 1st line - increases GI clearance of ammonia, decreasing absorption
  • Rifaximin - antibiotic that alters gut fauna, decreasing ammonia production
  • Liver transplantation if the above fail
93
Q

What is Budd-Chiari syndrome?

A
  • Hepatic vein thrombosis
  • Causes triad of symptoms:
    • Abdominal pain: sudden onset, severe
    • Ascites → abdominal distension
    • Tender hepatomegaly
94
Q

Diagnosis of Budd-Chiari syndrome?

A

Ultrasound with doppler flow studies

Emergency Medicine (20 decks)

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