A 35-year-old woman vomiting blood

Published on 10/04/2015 by admin

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Problem 35 A 35-year-old woman vomiting blood

Blood tests become available as follows:

Investigation 35.1 Summary of results

A further detailed history reveals that the woman has never vomited blood before but did have one episode of black stools 3 weeks earlier which she put down to diet. She has had no indigestion and has not taken any non-steroidal anti-inflammatories. She has never had any operations. Her partner volunteers that, up until 3 years ago, she had had longstanding problems with alcohol excess and had seen a hospital specialist who had warned her that she would die if she continued to drink. They had made a decision to move across the country to start a new life and she had not had an alcoholic drink since.

You organize an urgent endoscopy. The endoscopist finds a large amount of fresh and altered blood in the stomach. No bleeding source is identified in the stomach or the duodenum. Figure 35.1A, B shows the positive findings.

The endoscopist places four bands on the varices, with apparent haemostasis. She returns to the ward. It is now 11 p.m.

At 5 a.m. you are called to the ward. The woman has had no further haematemesis. She has become confused and is trying to remove intravenous cannulae and get out of her bed. Her blood pressure is 120/79 mmHg, her pulse 90 and her SpO2 98% on room air. She has had 3 units of FFP. A fourth unit of packed cells is running.

Shortly after your arrival, she has a further large haematemesis. Her GCS is 11. Her pulse has risen to 130 and her blood pressure fallen to 86/49 mmHg. She is sweaty and peripherally cool. The nurses and her husband are very concerned and look to you for answers.

The woman is taken to the endoscopy suite once more. Copious fresh blood is seen in the oesophagus. Despite their best efforts, haemostasis cannot be achieved. A balloon tamponade tube is inserted with airway control. The patient is taken to the intensive care unit.

The following morning a definitive procedure is performed. An image taken from this procedure is shown (Figure 35.2).

Three days later the woman is discharged. Two years later, she remains well. She works full time as a chef and has had no further bleeding.

Answers

A.1 The patient has had a significant upper GI bleed with a very large witnessed haematemesis. Despite her young age, she is already showing signs of shock with a tachycardia. Her airway may be at risk if she vomits further. High-flow oxygen should be administered. Intravenous access with two large-bore cannulae should be secured. Blood should be taken immediately for a 6 unit cross-match, full blood count, clotting, electrolytes and liver enzymes. Intravenous fluids can be used to restore circulating volumes although note cautions later. There are many debates about the best fluids to use (crystalloid vs colloid) but there is no doubt that the best of all in this situation is blood.

A.2 You will want to know any previous medical history including previous GI bleeding, peptic ulceration or liver disease. Has this happened before? Has it been accompanied by abdominal pain or dyspepsia, suggestive of a peptic cause? Did she have ‘normal’ vomitus before bringing up blood? This may suggest a Mallory–Weiss tear following trauma to the oesophageal mucosa. This can produce surprisingly brisk haemorrhage. Does she take any culpable medications including often short courses of non-steroidals or aspirin. Has she had melaena? The absence of melaena in the context of a large haematemesis normally implies an oesophageal source.

A.3 She has a very mild anaemia. This is often overtly reassuring but remember! In the acute stages of any form of bleeding the haemoglobin concentration is initially well maintained until haemodilution occurs. Haemoglobin concentration is not the same as total haemoglobin so do not be falsely reassured. Her platelet count is very low. While there are many causes, it may signify hypersplenism and, therefore, portal hypertension and liver disease.

There is further evidence of this in her liver synthetic function. She has a slightly increased prothrombin time and a mildly depressed albumin. In addition she has minor abnormality of her liver enzymes.

The urea : creatinine ratio is helpful in ascertaining the source of any GI bleed. In this case, we know from her presentation that it is upper GI. However, in cases of melaena or passage of fresher blood rectally, this ratio can be helpful. The sudden appearance of a high protein load in the upper gut generates a high level of blood urea in upper GI blood loss. Later, this becomes relevant in this case.

The woman needs an endoscopy urgently. In view of the possibility of variceal haemorrhage, the patient is likely to need a general anaesthetic for airway protection. You may want to consider platelet transfusion.

A.4 This information makes the presence of significant liver disease and, therefore, a variceal bleed, all the more likely. Variceal bleeding is an endoscopic emergency. You may even want to consider giving a potent vasoconstrictor such as terlipressin if endoscopy is likely to be delayed. Get advice now. Antibiotics may need to be considered. Beware over-zealous volume resuscitation. (See later to find out why.)

A.5 These are endoscopic images of the lower oesophagus: four variceal cords are seen. There are several ‘red spots’ which are signs of high-risk bleeding points although no active bleeding is currently seen. The endoscopist rightly asserts that the bleeding has come from the varices and places bands on the varices endoscopically. There is good evidence that this technique is significantly superior to older ‘injection’ sclerotherapy.

A.6 In variceal bleeding, broad-spectrum antibiotics reduce septic complications and short-term mortality. If bleeding has not been reliably controlled, terlipressin may be required but this drug is a potent vasoconstrictor and can cause ischaemic complications if not used with care. She is now at risk of hepatic decompensation.

A.7 First consider the possible latent effects of sedative or anaesthetic agents especially in a patient with liver disease in whom these drugs are often metabolized extremely slowly. However, she has emptied a large ‘high protein load’ into her gut – i.e. blood. This provides a substrate for gut bacteria to produce ammonia.

Ammonia, and associated by-products of protein metabolism, may enter the systemic circulation via the portosystemic shunts, of which her varices are examples, which define portal hypertension. In addition, poor synthetic function means that ammonia entering the liver via the portal circulation will not be adequately metabolized. This then causes hepatic encephalopathy.

Hepatic encephalopathy may have been precipitated by drugs, as above, or signify further bleeding. A patient in this situation is at risk of losing airway control. Further sedatives are not appropriate outside a high dependency/intensive care environment. Aperients such as lactulose may be useful later on.

A.8 The situation has deteriorated significantly and she is now in grave danger. She needs to be intubated and taken to ITU as soon as possible. If not already given, a vasoconstrictor such as terlipressin should be administered.

It is quite likely that over-enthusiastic fluid resuscitation has led to a rise in her portal pressure to provoke further bleeding. Once stabilized, she will need a further endoscopy.

A.9 This is a transjugular portosystemic shunt stent or TIPSS. The metallic stent is seen lying between the hepatic veins and portal vein in an artificially created channel. The radiologist has also inserted some metallic coils into one of the collateral vessels feeding her bleeding varices.

Revision Points

Management of Variceal Haemorrhage

Further Information

, http://www.patient.co.uk/doctor/Upper-Gastrointestinal-Bleeding.htm. A decent article on upper GI bleeding with a useful ‘calculator’

, www.daveproject.org. An excellent online source of fascinating endoscopy videos