Approach to UBGIT Flashcards
What is UBGIT?
Bleeding that occurs proximal to the ligament of Treitz, a ligament which is a suspensory muscle of the duodenum that connects DJ flexure to surrounding celiac axis and SMA
What is the clinical presentation of UBGIT?
Hematemesis and melena
Might present with hemorrhagic shock
Spectrum corresponds to rate of bleeding - red hematemesis/frank PR bleeding indicates faster rate of bleeding
What are the factors that predict UBGIT?
- Melena in history/examination
- Blood or coffee ground vomitus in NG lavage
- BUN :serum CR >30
*Presence of blood clots in stool make UBGIT less likely
What must be elicited in taking history of UBGIT?
- Nature of bleeding - Hemoptysis or UBGIT?
- Eitology - Variceal or non variceal?
- Quantify amount of bleeding
- Comorbidities
How do you confirm UBGIT in history?
Hemoptysis vs Hematemesis
Hemoptysis - associated with cough, sensation in throat before coughing frothy, fresh, bright red blood without any melena
Hematemesis - not associated with cough, not frothy, darker red (due to HCL) and presents with melena
How do you discern between Melena and Frank PR bleeding?
2 types of Melena
Fresh melena - Jet black with sheen, tarry, liquid consistency, non particulate
Stale melena - black-grey, mixed with stool, occasionally particulate
Must rule out iron in stool - which will produce a greenish hue on rubbing. Mix in water to confirm - melena will turn water black, iron will turn water green
Frank PR bleeding
-Very brisk upper GI bleeding, if presenting with hemodynamic instability might indicate severe bleeding
What in the history would suggest variceal bleeding?
Variceal vs non variceal bleed
Variceal bleed - ask for
- History of variceal bleed
- Liver disease/ risk factors for liver disease - alcohol, hepatitis
What are the types of non variceal bleeding?
- Peptic Ulcer Disease (most common cause)
● History of dyspepsia, previous H. pylori infections, previous endoscopy (OGD) performed
● Drug History – NSAIDs, antiplatelets, steroids, anticoagulants, TCM
● Secondary to cirrhosis-induced hypergastrinemia from decreased hepatic metabolism of GI hormones
- Stress Ulcer
● Curling ulcer – large acute ulcer in the duodenum (cx from burns) – can cause mucosal ischemia
● Cushing’s ulcer – gastric ulcer produced by elevated ICP (i.e. head trauma) – vagal stimulation leads to increased Ach &
H+ production
- Mallory-Weiss tear
● Diagnosis requires a high index of suspicion
● Characterized by arterial bleeding (hematemesis or melena – depending on volume), secondary to violent retching following
alcoholic binge (rapid increase of intra-abdominal and intraluminal gastric pressure).
● This leads to one or more longitudinal fissures in the mucosa of the herniated stomach at the GEJ
● Majority of bleed with stop spontaneously with non-operative management (decompress stomach and give antiemetics) - Dieulafoy’s Disease - a medical condition characterized by a large tortuous arteriole most commonly in the stomach wall (submucosal) that erodes and bleeds
● Presents with massive or recurrent bleeding coming from an area of apparently normal gastric mucosa.
● Characterized by a large tortuous arteriole in the submucosal that bleeds
● More common in males, with multiple comorbid (i.e. HTN, IHD, ESRF, DM)
● Suspect in patients presenting with BGIT with no history of alcohol abuse or NSAIDs use - Malignancy (gastric / oesophageal carcinoma)
● Early lesions: asymptomatic, epigastric pain, dyspepsia
● Intermediate lesions: anemia, melena, hematemesis, early satiety, dysphagia, nausea/vomiting, bloatedness
● Late lesions: loss of appetite, loss of weight, palpable epigastric mass, obstructive jaundice (mets to liver) - Gastric Antral Vascular Ectasia (dilation or distention of a tubular structure)
● Dilated mucosal blood vessels that often contain thrombi in the lamina propria (predominantly affects distal stomach),
appears as longitudinal linear red streaks on the antrum mucosa (i.e. watermelon stomach)
● More common in elderly women with chronic occult GI blood loss
● Associated with autoimmune connective tissue disorder and/or chronic liver disease
How do you quantify the bleed?
If the patient presents with haematemesis, ask how much blood vomited, Cup? Bowl?
- When patients have hematemesis, there can by up to 1.5L of blood in the stomach (bleeding more than pylorus can empty)
- Is patient symptomatic from BGIT, any symptoms of chest pain, shortness of breath
- Gauge percentage of blood loss
● 15-30% 🡪 class 2 – Narrowed Pulse Pressure, Resting Tachycardia, Postural Hypotension
● 30-40% 🡪 class 3 – Supine Hypotension, marked tachypnoea, confused, anxious
● > 40% 🡪 class 4 – Minimal urine output, markedly depressed or lethargic
What are the other comorbidities associated with UBGIT?
Ask about other significant medical history, of importance is cardiac history, renal history
● Presence of IHD/CCF will predispose patients to fluid overload during resuscitation
● Presence of ESRF will predispose patients to fluid overload during resuscitation
- Ask about other significant medication history
● Presence of antiplatelets, anticoagulants, novel oral anticoagulants (should be stopped in acute bleed)
● Presence of anti-hypertensive medications (should be stopped in acute bleed), Beta-blockers can mask tachycardic
response
● Is patient previously on any proton pump inhibitors or H2 antagonist
What are the important clinical examination for UBGIT?
- Vital signs
- Confirm UBGIT with DRE/NG lavage
- Determine eitology if it is variceal bleed with stigmata of chronic liver disease
- Look for complications
Anemia:
Face - conjunctival pallor of mucos membrane
Cardiac auscultation of short systolic flow murmur at aortic area
Pulse with tachycardia, bounding or collapsing pulse
Hands with pallor
Urine output low
Lungs for possible aspiration pneumonia
Exclude peritonism - contraindication for endoscopy
What are the differentials for UBGIT?
What is the immediate management for a patient with UBGIT
- Fluid resucitation
- Adjunct
- Early Medication
- Urgent OGD
Fluid Resuscitation
- Assessment begins with Airway, Breathing & Circulation
- If patients can respond logically, his airway and breathing is intact. Logical responses also suggest good cerebral perfusion. If
airway or breathing is affected, consider early intubation to protect the airway from risk of aspiration pneumonia
- Circulation: even if patient appears to be hemodynamically stable, he may be in class 1 hypovolemic shock, management should
be pre-emptive
● Nasal Prongs (supplemental O2 to increase O2 carrying capacity)
● IV cannula: 2 large bore 18G catheter inserted at the antecubital fossa
● IV cannula sizes: 14G – orange, 16G – grey, 18G, green, 20G, pink, 22G, Blue, 24G – yellow
● Bloods should also be taken for investigations: GXM, FBC, U/E/Cr, PT/PTT/INR, LFT, Trop I
○ GXM: needed prior to ordering of cross-matched bloods
○ FBC: assessment of hemoglobin level (compare against the baseline), assessment of platelet level (any risk of bleeding)
○ U/E/Cr: assessment of urea level (isolated uremia suggestive of UBGIT), assessment of creatinine or eGFR (may
require contrasted scans to investigate bleeding)
○ PT/PTT/INR: assessment of degree of coagulopathy (especially important for patients on anticoagulants)
○ LFTs: deranged in patients with chronic liver disease, suggestive of possible variceal etiology
○ Trop I: patients are at risk of developing T2MI with severe blood loss
○ ABG/Lactate: useful in patients presenting with hemodynamic instability / hypovolemic shock
● ECG to rule out cardiac event
- Circulation: if patient is hemodynamically unstable
● Fluid resuscitation with crystalloids / ± colloids / packed cells / platelets / FFP
● Run in 1L N/S fast (i.e. over 15 mins) and assess clinical response
○ Responder: sustained improvement clinically & biochemically
○ Transient responder: transfuse blood products, if unavailable, can consider colloids
○ Non-responder: E-bloods (may require massive transfusion protocol)
● Restrictive transfusion strategy to keep Hb > 7g/dL (showed improved outcomes as compared to liberal transfusion strategy
[transfusion when Hb < 9] in patients with acute UBGIT) 65
● May consider platelets if patient has quantitative (i.e. <50k) or qualitative (i.e. on antiplatelets) deficits
● FFP if patient is on anticoagulants or PT/PTT prolonged (+/- IV vitamin K) - refer to protocol
- NG tube if patient is having hematemesis – prevents aspiration, allows gastric lavage prior to OGD (DO NOT insert if suspect
varices) – can also be used to confirm suspicion of UBGIT - Arterial Line / CVP – for monitoring of hemodynamic status
IDC insertion – monitor I/O balance esp. in elderly or when large amount of fluid resuscitation required, or anticipating surgery
- Intubate if patient having massive uncontrolled active hematemesis or signs of decompensation
- Targets: Keep MAP: > 60mmHg (for end-organ perfusion), urine output > 0.5ml / kg / hr & Hb: ≥ 7 or ≥ 9 (IHD)
- Early medications
- IV omeprazole 80mg bolus followed by 8mg/hr for 3 days (decreases stomach pH which helps in stabilizing clot formation)
- If suspecting varices – IV somatostatin 250mcg followed by 250 mcg/hr &, IV ceftriaxone 1gm once
- If planning for urgent endoscopy, KIV for IV erythromycin (for gastric emptying)
- Withhold all antiplatelets, anticoagulants,NOAC, NSAIDS, anti-hypertensive - Urgent esophagogastroduodenoscopy (OGD)
- Indications: - Hemodynamic instability despite fluid resuscitation (ensure BP is stable before OGD – requires sedation)
- Active BGIT, in patients presenting with hematemesis and/or fresh melena
- Suspected variceal bleed (bleeding can be brisk)
- Risks / Benefits
● Anaesthetic Risk: Risk of Sedation – respiratory depression secondary to airway compromise. CVS risk – AMI, CVA
● Procedural-Related Risk
○ Bleeding and Perforation (1 in 10,000)
○ Failure of endoscopic haemostasis
○ Failure of complete scope – standard OGD scope to D2
● Benefits: OGD will help to diagnose the source of bleeding, enable therapeutic procedures to be carried out and allows for
prognostication of re-bleeding
- Patients whose condition does not stabilize after initial resuscitation (i.e. hypovolemic shock), proceed for urgent endoscopy.
- However, if patients are high risk (i.e Glasgow–Blatchford score of ≥ 12) but hemodynamically stable, endoscopy performed
within 6 hours after GI consultation was not associated with lower 30-day mortality than endoscopy performed between 6 and 24
hours after consultation.66
Why is somatostatin used in variceal bleeding
It causes vasoconstriction of the portal venous SYSTEM
