Emergency General Surgery

Game of Thrombosis

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Let’s start with something we are extremely used to:

You are on call, it’s evening, and your shift is about to finish, but you decide to visit this last patient who is waiting patiently outside your ambulatory for 3 h with his green card (triage color) in his hands. When he comes inside your room, he is holding his belly like a massive pain is driving him crazy. He complains of this acute but vague abdominal pain that popped up right after lunch. He vomited, but the pain is still there. He is 75 yo, he is on warfarin for atrial fibrillation and he underwent a left colectomy for cancer 7 years ago. On medical examination the abdomen is not tender, palpation doesn’t increase or worsen the pain, peristalsis is present, Murphy’s and Blumberg’s signs are negative. Rectal exploration reveals normal stool in the ampulla. 

Your nurse gets an IV line and starts paracetamol as a painkiller.

A few minutes later (we know, it’s impossible but this is a case scenario) your laboratory results come back: Ht 45%; Hb 15 g/dL; WCC 16.000 mm3; CRP 1 mg/l; Lac 3; BE -2; INR 2.3; aPTT 0.93.

Now? What do you think? What are your differential diagnoses?

This is the classic presentation of a patient with suspected mesenteric ischemia. We know we forced the presentation a bit with already some topical clinical findings, but if you’re not suspecting it you will surely miss the diagnosis. 

Acute mesenteric ischemia (AMI) is a pathology we all fear and struggle to diagnose. It is rare, but the presenting symptoms are vague. 

How many “senior” patients with vague abdominal pain do we see in a day when on call? But how many of them do risk having mesenteric ischemia?

We stress this point: the key to early diagnosis is a high level of clinical suspicion. Almost all of our patients will come to our ED reporting abdominal pain (acute or chronic – we’ll see the difference), nausea, vomiting, and, sometimes, diarrhea. 

Giving a definition, AMI is a sudden interruption of blood supply to a segment of the intestine, leading to ischemia, necrosis, and, if left untreated, to patient death. 

We need to bear in mind that almost 25% of the cardiac output goes to the splanchnic circulation at rest and it increases to 35% in the post-prandial phase. From animal studies, we know the gut can survive a 75% reduction in blood flow for up to 12 h without significant injuries. However, its viability drops to 54% between 12 and 24 h, and to 18% after 24 h.

The diagnosis is difficult and failure in recognizing an ischemic bowel is the main responsible for the high mortality of this disease. The mortality rate remains high, ranging between 50 and 69%. The mortality is related to treatment timing: the later you diagnose it, the higher the patient’s risk!

Your first steps in a patient with the clinical suspicion of AMI will be:

  • Ask for laboratory tests: none of your lab-test alone will be sufficient for the diagnosis. Most patients present laboratory abnormalities such as hemoconcentration, leukocytosis, metabolic acidosis with a high level of lactates, serum amylase, aspartate aminotransferase, lactate dehydrogenase, and/or creatine phosphokinase. Remember that in a patient with acute abdominal pain, a normal serum lactate level should not be used to rule out AMI, while a high level of lactates (>2 mmol/l) are generally associated with irreversible intestinal ischemia and high mortality. Yet, it could also mean “simple” hypoperfusion.
  • Do a POCUS (point of care ultrasound): this is your pre-first-line imaging tool. It might be helpful to differentiate a small bowel obstruction, where bowel spasms and a sonographic “to and fro” motion of the bowel can be recognized, from an advanced AMI, where signs of intestinal mobility might be absent due to extended necrosis. Moreover, intraperitoneal fluid is often detected by ultrasound and a sample of the fluid might be obtained through a US-guided diagnostic peritoneal aspiration (DPA).
  • Ask for a CT-angio (CTA) of the abdomen: Every patient suspected of AMI needs a CTA! It is the gold standard and the first-line imaging method, and it should be obtained as soon as possible when AMI is suspected. The most favorable outcome is strictly related to time to surgery. Due to high mortality, CTA should be performed immediately also in case of patients with renal failure, as the consequences of a delayed or wrong diagnosis are far more detrimental to the patient than the exposure to contrast media itself. CTA plays an important role not only for its high diagnostic accuracy but also for its capacity of detecting other causes of acute abdominal pain. Furthermore, this method is fundamental to determine the causes of AMI. Specific features of AMI on CTA are:
    • The appearance of bowel wall thickening;
    • Bowel dilation;
    • Occlusion of mesenteric vessels;
    • Mesenteric haziness;
    • Intestinal pneumatosis and portal venous gas;
    • Intraperitoneal fluid;
    • Pneumatosis intestinalis.

Finally, we have the diagnosis, and our patient has AMI… what now?!

What we should do is start the basic patient support principles. One of the main goals of resuscitation is the restoration of adequate tissue/organ perfusion and they can be summarized in the three Rs: Resuscitation, Rapid diagnosis, Revascularization. 

Resuscitation accounts for adequate blood volume and oxygenation. Supplementary oxygen should be given, and fluids should be started. Do not use colloids to resuscitate your patient! A recent Cochrane Review showed no advantages of colloids over crystalloids in reducing mortality. Moreover, evidence suggests that the use of hydroxyethyl starch might increase mortality.

Check for electrolyte levels and metabolic status. In case of severe metabolic acidosis and hyperkaliemia, due to bowel infarction and/or reperfusion syndrome, they should be corrected. Nasogastric decompression should be considered as well.

Vasopressors reduce splanchnic perfusion and should be avoided whenever possible. When required, consideration should be given to drugs that have fewer effects on the mesenteric blood flow as dobutamine, low dose dopamine, and milrinone. 

Broad-spectrum antibiotics should be given since intestinal ischemia leads to early loss of mucosal barrier, which facilitates bacterial translocation and risk of septic complications. 

There are some differences in presentation, diagnosis, and treatment according to the etiology of AMI. Let’s see them…

Embolic Acute Mesenteric Ischemia (EAMI)

Arterial embolism is the most frequent cause of AMI (i.e. 45%). 

The classic patient reports the acute onset of abdominal pain associated with vomiting and/or nausea. The pain is abnormal compared to the clinical examination. Usually, atrial fibrillation or other comorbidities such as ischemic heart disease, hypertension, diabetes mellitus, and renal failure are present. 

The majority of emboli lodges at the origin of the superior mesenteric artery (SMA), meaning the treatment needs to be interventional (open surgery or endovascular depending on the hospital’s skills and resources). Open embolectomy is still widely performed via a midline incision, approaching the SMA just below the pancreas, at the root of the mesentery. On the other hand, endovascular embolectomy has become more common owing to the development of dedicated catheters. The caveat accompanying the endovascular-first strategy is not to postpone laparotomy if symptoms do not resolve after successful embolus aspiration. If irreversible bowel necrosis has already developed, surgical exploration along with resection of necrotic tissue is mandatory. It is not unusual that occlusive AMI is followed by NOMI after revascularization.

Thrombotic Acute Mesenteric Ischemia (TAMI)

Arterial thrombosis is responsible for approximately 25% of AMI. 

Patients will complain of chronic abdominal pain exacerbating after eating, he/she may have “food-fear” with weight loss suggestive of undiagnosed chronic mesenteric ischemia. 

The main risk factors for TAMI are atherosclerotic disease and dyslipidemia. Moreover, patients might report previous vascular events or vascular surgery. Thrombosis occurs at the origin of visceral arteries, and an underlying plaque in the SMA usually progresses to critical stenosis over years, resulting in collateral arterial supplies. The involvement of the ileocolic artery will result in necrosis of the proximal colon. 

As for the EAMI, the treatment is based on endovascular stenting or surgical vascular bypass. Endovascular treatment should be the first choice for TAMI whenever possible and should be done as soon as possible. It should be performed before intestinal infarction occurs and when the ischemia is still potentially reversible. The commonest interventions are percutaneous transluminal angioplasty with/without stenting. Other endovascular techniques include percutaneous aspiration thrombectomy, local fibrinolysis, or intra-arterial drug infusion (such as heparin or papaverine). 

Surgery may be needed to resect the ischemic bowel before the vascular intervention or when percutaneous treatment has failed. Possible surgical options for revascularization are thromboendarterectomy, reimplantation of the SMA, SMA bypass, and retrograde open mesenteric stenting (ROMS). Among them, ROMS should be generally preferred, but it requires technical expertise. When the patient is in extremis, the operation time should be kept to a minimum. Where vascular expertise is not available, it may be reasonable to resect the necrotic bowel first and transfer the patient for urgent interventional angiography or vascular surgery.

The choice of open versus endovascular versus hybrid technique must be based on the long-term patency of the arterial supply since it’s known to be lower after stenting rather than after surgical procedures. 

Approximately 30% of patients treated with endovascular techniques require a second angioplasty during the following 2 years.

Venous Acute Mesenteric Ischemia (VAMI)

Venous thrombosis represents 10% of patients with AMI and it usually occurs in a younger population (over 40 yo). It is frequently associated with hypercoagulable states (e.g. protein C and S deficiency, polycythemia, Leiden factor V mutation), cirrhosis or portal hypertension, severe pancreatitis, nephrotic syndrome, abdominal trauma, and advanced malignancy, although it may be idiopathic. Oral contraceptives, pregnancy, and puerperium are risk factors in young women. Up to 50% of patients report previous deep thrombosis or pulmonary embolism. 

The onset of VAMI is characterized by vague subacute abdominal pain that may develop over a period of up to 2 weeks. Half of the patients will complain of nausea and vomiting. In these cases, the first-line therapy is based on heparin (continuous infusion versus low-molecular-weight). A second step may be endovascular or surgical; yet, it is usually managed without surgery. Anticoagulation with continuous infusion of unfractionated or low-molecular-weight heparin is the first-line treatment for VAMI and should also be started in case of intraoperative diagnosis. Isolated thrombosis of the superior mesenteric vein is usually compensated by sufficient collateral circulation. However, additional complete thrombosis of the portal vein leads to venous infarction of small bowel loops of different severities, and it may require laparotomy. 

Non-Occlusive Mesenteric Ischemia (NOMI)

It accounts for approximately 20% of cases of mesenteric ischemia. It is often silent as it occurs in critically ill patients often sedated and ventilated in the ICU. Pathophysiology is poorly understood, but it can be explained by a combination of low cardiac output and vasoconstriction. Hypovolemia and the use of vasopressors may precipitate NOMI. Risk factors are age over 50 yo, history of acute myocardial infarction, congestive heart failure, aortic insufficiency, cardiopulmonary bypass, renal or liver disease, or major abdominal surgery. It should be suspected in patients with mesenteric hypoperfusion secondary to circulatory shock or vasoactive drugs. Acute or insidious pain, constipation, bloating, and the presence of blood in the stools are all consistent with NOMI in critically ill patients. Most patients will display symptoms of abdominal sepsis associated with abdominal distension as late clinical signs. Beware that sometimes patients may not show any symptoms because of the sedation administered in the ICU.

The treatment of NOMI is based on correcting the clinical or pharmacological conditions that generate splanchnic vasoconstriction, improving mesenteric perfusion, and early recognition and resection of infarcted bowel. 

The main factor in improving mesenteric perfusion is the restoration of circulatory volume and hemodynamic stability along with the use of vasodilators administered directly into the SMA to reverse the intestinal vasospasm that causes the ischemia. 

TYPECAUSEMEDICAL HISTORYPAINBOWEL INVOLVED
EAMIEmbolusAtrial fibrillation, endocarditis, mitral valve disease, previous embolic diseaseAcute onsetMid-gut (tipically sparing the proximal jejunum and colon)
TAMIAtherosclerosis, vasculitis, mycotic aneurysmPrevious angina abdominisRecurrentWhole small bowel and proximal colon
VAMICoagulation disordersPrevious DVT and/or PE, oral contraceptives, younger patientsGradual and insidiousWhole small bowel and proximal colon
NOMIVasopressorsICU patients (low cardiac output, EN on going)Insidious (sedation)Proximal colon

A minimally invasive approach (i.e. laparoscopy) should be taken into account when facing unclear scenarios. It may avoid a laparotomy and still lead to a correct diagnosis. It should be used in patients with normal hemodynamic status and clinical suspicion of abdominal pathology when laboratory tests and imaging are not diagnostic. One limit would be the inability to fully explore the abdomen and the whole bowel, even though this risk can be mitigated by the surgeon’s experience and skill. 

To increase the sensibility and specificity of the procedure, indocyanine green fluorescence can be used. 

Another use of laparoscopy should be in unstable patients, where the extent of ischemic bowel may lead to a damage control procedure or a palliative approach. The laparoscopic camera may also be set up in the ICU and may help the surgeon to decide the next move. 

Damage Control Surgery (DCS) & Open Abdomen

Patients with AMI who have severe sepsis or septic shock should undergo damage control surgery (DCS). The decision to opt for DCS should be made early during surgery, or even before starting it. It should be based on the patient’s response to resuscitation and ongoing physiology. Advanced age is not a contraindication to DCS, as good outcomes have been observed in the elderly. 

A bowel anastomosis should be performed only in well resuscitated and stable patients, where there is no doubt about the viability of the bowel. During the first operation, only the clearly necrotic areas should be resected. A second look operation should then be taken into account in every situation where the patient’s physiology is unstable (i.e. damage control surgery) or when the viability of the bowel is unsure (e.g. after a SMA bypass) or when the patient may need an angiography procedure after the laparotomy. In each scenario, it is useful to check again the bowel viability after proper resuscitation. The timing for the second look should be within 48 h, but not before 24 h. If multiple relook procedures are needed and the bowel viability is still uncertain, bowel exteriorization should be considered as a valid option.

When leaving the abdomen open, recent evidence suggests the use of the peritoneal resuscitation technique may aid in restoring normal bowel appearance and general physiology before the second look. 

Futile Care

Resection of the entire ischemic bowel may result in short bowel syndrome (SBS) with its serious associated consequences, especially when the bowel left is shorter than 200 cm. This may not be an optimal state, particularly in elderly and infirm patients, who may not tolerate long-term parenteral nutrition. 

In this particular and challenging decision-making process, the use of a clinical frailty scale might be helpful also to discuss the clinical scenario with the patient’s relatives, thus avoiding misleading expectations.

The benefit of extensive small bowel resection should be balanced against the resultant quality of life, morbidity, and mortality, especially in elderly patients. 

We hope you have enjoyed this quick overview of this rare but troublesome problem.

See you next time folks…

Namastè…

Acknowledgement

Many thanks to our dear friend Hayato Kurihara for his contribution to writing this post.

References
  1. Kärkkäinen JM, et al. Acute mesenteric ischemia (Part II) – Vascular and endovascular surgical approaches. Best Practice & Research Clinical Gastroenterology 2017;31:27–38.
  2. Bala M, et al. Acute mesenteric ischemia: guidelines of the World Society of Emergency Surgery. World J Emerg Surg. 2017;12:38.
  3. Garzelli L, et al. Contrast-Enhanced CT for the Diagnosis of Acute Mesenteric Ischemia. American Journal of Roentgenology 2020;215:29-38.
  4. Tilsed JVT, et al. ESTES guidelines: acute mesenteric ischaemia. Eur J Trauma Emerg Surg 2016;42:253-70.
  5. Acosta S, et al. Open abdomen in acute mesenteric ischemia. Anaesthesiol Intensive Ther 2019;51:159-62.
  6. Bryski MG, et al. Techniques for intraoperative evaluation of bowel viability in mesenteric ischemia: a review. Am J Surg 2020;220:309-15.
  7. Furukawa A, et al. CT diagnosis of acute mesenteric ischemia from various causes. Am J Roentgenol 2009;192:408-16.
  8. Reginelli A, et al. Intestinal Ischemia: US-CT findings correlations. Crit Ultrasound J 2013;5:S7. DOI:10.1186/2036-7902-5-S1-S7.
How to Cite This Post

Kurihara H, Marrano E, Bellio G. Game of Thrombosis. Surgical Pizza. Published on March 6, 2021. Accessed on May 5, 2021. Available at [https://surgicalpizza.org/emergency-surgery/game-of-thrombosis/].

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