Acute Abdominal Aortic Occlusions

Transcription

1 Acute Abdominal Aortic Occlusions G. Szendro O. Mayzler G. Greenberg V. Ginzburg A. Leytzin L.I.V.E 2018 Soroka Medical Center Ben-Gurion University Beer Sheva Israel

2 Acute Aortic Occlusions - AAO Acute aortic occlusion is a rare but a catastrophic emergency condition which is easily overlooked by non vascular experts. When overlooked it has poor prognosis. Despite having a characteristic presentation delayed diagnosis is not uncommon. The clinical presentation may vary from acute limb ischemia, neurological symptoms of the pelvis and lower extremities, abdominal symptoms and acute hypertension. Early recognition and intervention are essential.

3 First time I came across the catastrophic First time I came across the catastrophic delays in the diagnosis and treatment of this pathology was in 1996 and published in the Annals of Oncology. delay in the diagnosis and treatment of this pathology was in 1995 and published in the Annals of Oncology.

4 Levels of AAO Slow onset of gradual occlusion and blunt trauma victims will not be discussed here. AAO can occur at various levels: Suprarenal Juxtarenal Infrarenal Bifurcation The higher the level, the more dramatic is the clinical presentation.

5 The higher the level, the more dramatic is the clinical presentation

6 Etiologies Embolism Thrombosis (Dissections( Contributing factors Heart disease Pre-existing atherosclerosis Low flow with poor cardiac output Hypercoagulable states Poor outflow & runoff

7 Rare causes Occasionally bizzare and super rare pathologies can lead to AAO like a case report from JVS 1992 when the aortic occlusion was produced by extrinsic compression of the Juxtarenal aorta from a closed loop small bowel obstruction contained within a peritoneal encapsulation.

8 Why is the M&M so high? Delayed diagnosis Delayed treatment Poor outcome Neurologic deficits are seen in 55%

9 Missed Diagnoses up to 50% Because it can mimic: Stroke Acute abdomen Acute back pain Sudden onset hypertension Spinal cord compression syndrome (Acute compressive myelopathy) Demyelinating polyneuropathy Qauda Equina Syndrome Paraparesis Paraplegia Dropfoot

10 Common involved disciplines Neurology/Neurosurgery/Orthopedics The long neurologic DD list represent either or both spinal cord ischemia and peripheral ischemic neuropathy. The diagnosis of abdominal aortic occlusion in acute paraplegia is missed in up to 50% of cases!!!!!!!!!!!!!!

11 Typical possible mis-investigation 67yo, male, smoker, diabetic, HTN, CIHD, lymphoma From case reports in neurological medicine Kilany et.al 2015 MRI of lumbar and thoracic spine Nerve conduction study X 2 results suggesting demyelinization and axonal damage Lumbar puncture Tumor markers for malignancy Non-contrast CT of chest, pelvis and lumbosacral spine >>Chest pain Coronary angiography via Radial A. PTCA performed CTA performed two days later due to toe discoloration Bilateral amputation Death

12 Cancer Patients - Facts I All active cancer patients are in hypercoagulable state (X4.5) II Chemotherapy causes hypercoagulopathy (X6) III Cisplatinum has the highest risk for thromboembolic events

13 Cont. Among 932 cancer patients at Memorial Sloan Kettering cancer center arterial thromboembolic events occurred in 8.3% Russel, Moore, Adel et.al American Society of Clinical Oncology

14 Cisplatinum Cisplatin, is the corner-stone agent in the treatment of a variety of malignancies, such as carcinomas of the ovary, GIT, lung, lymphomas, sarcomas, germ cell tumors and others. One of the most important complications of cisplatin-based chemotherapy is the high risk of thromboembolic events, namely cardiovascular complications.

15 Among those CV complications, AAO in non atherosclerotic vessels are possible and are of special interest. Chemotherapy has been postulated as an independent risk factor for thrombosis by way of cytokine activation, direct toxic effect on blood vessels and disruption of the balance between procoagulant and anticoagulant factors.

16 Cont. Additional possible Cisplatinum thrombogenic effects are: * Elevated plasma Von Willebrand factor levels * Drug induced reduced LV function * Inducing hypomagnesemia causing vasospasm

17 Cont. Different chemotherapy agents have shown to affect thromboembolism differently. Platinum-based chemotherapy is shown to double the incidence. However, vascular complications occurring during Cisplatin-based chemotherapy are inadequately recognized even to date.

18 Diagnostic Options I II III Clinical suspicion Clinical suspicion Clinical suspicion Avoid delay in diagnosis Physical examination Duplex CTA/MRA Should also check visceral artery involvement THE CATASTROPHIC OUTCOME IS DIRECTLY RELATED TO DELAYED DIAGNOSIS

19 Therapeutic Options AVOID DELAY IN TREATMENT Endovascular Thrombolysis Thrombectomy Recanalization & Stenting Fasciotomy Amputation Operation Thrombectomy Ax-Bifem-Bypass Ao-Bifem-Bypass Especially when renals are involved

20 Cases AAO near aortic bifurcation

21 Thrombectomies & EV option E.V. OUTCOME

22 Acute atherosclerotic occlusion Juxta renal AAO. 3D image from posterior view 24 hour diagnostic delay Treated by Aorto-bi-femoral bypass

23 A recent juxtarenal occlusion treated by Ao-bi-femoral bypass + Fasciotomy

24 Recent AAO of an AUI STENTGRAFT Successfully treated with thrombolysis Posterior view Pre Lysis Post Lysis Thrombolysis Only TPA >> Urokinase

25 Not all Cisplatinum related Aortic thromboses cause total occlusions and are so dramatic and urging immediate interventions. Cisplatinum induced Aortic thromboses can be with only mild to moderate consequences ending with anticoagulation alone.

26 3 total AAO Case Histories a. All receiving Cisplatinum b. All with sudden onset of LL plegia/paresis c. All with Cauda Equina syndrome without preceding significant ischemic leg pain.

27 Cont. 1. Small cell lung ca. 2. Small cell lung ca 3. Squamous cell nasopharyngeal ca Latent period between Tx and clinical presentation a few days. Absent femoral pulses missed for days. Spinal cord metastatic compression investigated and treated in one case before ischemia was realized. Appropriate vascular investigation only after feet discoloration. In one case >>>>> Bilateral AKA.

28 Representative Cis. case 48 h delay. 56 y.o female with lung ca. Last Cisplatinum Tx -8 days ago st ER visit with paraparesis and calf pain Discharged nd ER visit with parapresis, LL hypoesthesia, Perineal hypoesthesia and urinary retention. CTA performed and successful emergency EV revascularization conducted.

29 Outcome per literature Diagnostic delays Mean: 18 hours Therapeutic delays < 24 h 55% > 24h 45% Procedure types Mentioned already Amputation rates: 20% (Crawford et.al JVS 14) higher rate in non claudicants Mortality rates 31% (in emboli 38% Vs Different Data 25-75% 29% in thrombosis - Robinson) 52% by Babu JVS % in poor LV, 23% in good LV

30 Cont. Crawford et.al JVS 2014 Hypercoagulability APLA in 17% Cancer induced in 23% Mortality 42% in hypercoagulable pts. 29% without hypercoagulability

31 Mortality per procedure Robinson et. Al. Ann. Vasc. Surg cases Trans femoral embolectomy (6) 50% Trans aortic thrombectomy (2) 100% Ax-bi-Femoral bypass (10) 30% Ao-bi-femoral bypass (6) 0% Endovascular (4) 25%

32 Lessons to be learnt AAO has occasionally a non typical presentation with misleading neurologic symptoms. This vascular pathology mandates the obvious of: * High level of suspicion * Detailed history * Complete physical examination including pulse palpation and ABI * Prompt diagnostic imaging * Urgent treatment Early diagnosis and treatment are the key to successful revascularization with minimal neurologic sequels.

33 Cont. Consider AAO when acute flaccid paraplegia occurs in the presence of severe pain at onset. Consider CTA even in the presence of distal pulsations. The biggest procedures do not have the highest mortalities. There is no current consensus on the use of thromboprophylaxis in patients receiving chemotherapy in general, let alone, those treated with Cisplatin derivates. Should it be changed???

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