Medical Image of the Month: Coccidioidal Pneumatocele Complicated by Pulmonary Hemorrhage

Figure 1. Axial CT of the chest without contrast 12 years prior to this hospitalization demonstrates an irregularly-marginated right upper lobe cyst measuring 1.5 x 1.6 cm (red arrow).

Figure 2. Axial CT of the chest without contrast obtained 4 months prior to this admission demonstrated a cavitary lesion now measuring 6.3 x 8.2 cm, thin-walled, with small internal air-fluid level and adjacent small pleural effusion without any internal debris (red arrow).

Figure 3. An axial CT angiogram of the chest in lung windows demonstrated a right upper lobe pulmonary cavitary lesion increased in size to 10.5 cm in largest dimension with almost complete opacification (red star) concerning for a superimposed infection.

A 77-year-old man with emphysema, hypertension, hypothyroidism, and diabetes mellitus presented with two days of worsening cough that progressed to massive hemoptysis. His hemoptysis included clots the size of golf balls and multiple episodes of frank blood, measuring half a cup each. His symptoms included dyspnea at rest, fatigue, and a 15-20-pound weight loss in three weeks. He denied fevers, night sweats, chest pain, hematemesis, and prior hemoptysis. Additionally, he had a history of coccidioidomycosis complicated by a cavitary lung lesion. Per chart review, 12 years prior to this hospitalization the patient had an irregularly-marginated right upper lobe cyst measuring 1.5 x 1.6 cm (Figure 1). A CT scan obtained 4 months prior to admission showed the cavity to be 6.3 x 8.2 cm thin-walled and clear of debris (Figure 2) – consistent with a pneumatocele. The patient was referred to thoracic surgery for possible resection at that time but was lost to follow up.

Admission labs showed a decrease in hemoglobin to 13.4 from a baseline of 15.1 g/dL and white blood cells of 10,300 cells/µL. Blood cultures were negative. CT angiography now demonstrated an increase in the right upper lobe pulmonary cavitary lesion to 10.5 cm in largest dimension with almost complete opacification of the lesion - concerning for a superimposed infection. Imaging also showed tree-in-bud nodules in right middle and lower lobes without evidence of a pulmonary embolism (Figure 3). Coccidioidomycosis serologies by EIA showed a non-reactive IgM with reactive IgG. Acid fast bacilli staining of the sputum was negative. Bronchoscopy performed in the hospital showed fresh blood present in the trachea and in the visualized tracheobronchial tree. Active bleeding was noted only from the posterior segment of the right upper lobe. A bronchoalveolar lavage was performed confirming alveolar hemorrhage centered in the right upper lobe. Lidocaine with epinephrine was instilled to stop bleeding. No endobronchial lesion was seen.

The case was evaluated by an interventional radiologist and cardiothoracic surgeon at our institution. They both felt the patient would benefit from transfer to a larger medical center for definitive management of his hemorrhage. He was transferred to a tertiary academic center for a right upper lobectomy, which he tolerated well.  Surgical pathology and bronchoscopy cultures ultimately grew coccidioides immitis and the patient was discharge on a treatment course of oral fluconazole.

Pulmonary pneumatoceles are thin-walled, air-filled cystic structures. Most pneumatoceles are encountered in infancy; however, they can appear at any age (1). Pneumatoceles are known sequelae of pneumonia but can also occur due to blunt thoracic injury or as a rare side effect of chemotherapy (2,3). While the mechanism of pneumatocele formation is unclear, several theories have been postulated including check-valve bronchial obstruction and narrowing or from parenchymal necrosis with accompanying focal collections of air within the interstitial tissue (5). Such cases are typically asymptomatic and do not require intervention as they resolve within weeks to months (6). While many pneumatocele resolve on their own without additional intervention, complex pneumatoceles may result in uncontrolled hemorrhage, as portrayed in this case, or infected lesions unresponsive to antibiotics - necessitating surgical intervention (7). Other complications of pneumatoceles are rare and may include a tension pneumatocele with cardiorespiratory compromise or pneumothorax (8). 

Staphylococcal pneumonia is frequently complicated by pneumatocele development, with pneumatoceles thought to occur in 61% of cases of staphylococcal pneumonia (9). However, the literature of pneumatocele development following cocci infection is scant. In immunocompetent hosts, infections from coccidiosis are transient, with pulmonary complications (often nodules and self-limited thin-walled cavities) occurring in less than 10% of patients (10).  Complications from coccidiosis infection are usually brief fatigue, dyspnea, cough, and arthritis, with chronic infection or severe complication being rare. Here, we report a case of a gradually enlarging pneumatocele in the setting of cocci infection that eventually eroded into the pulmonary vasculature. The resulting massive hemoptysis was refractory to epinephrine injection and not amenable to catheter embolization. Upper lobectomy was required for definite treatment of the pulmonary hemorrhage.

Sylvester Moses MD, Gregory Gardner MD, Ella Starobinska MD, and Arthur Wolff MD

Department of Internal Medicine

University of Arizona

Tucson, AZ USA

References

1. Flaherty RA, Keegan JM, Sturtevant HN. Post-pneumonic pulmonary pneumatoceles. Radiology. 1960;74:50-3. [CrossRef] [PubMed]
2. Aissaoui O, Alharrar R. Traumatic pulmonary pseudocyst: a rare complication of blunt thoracic injury. Pan Afr Med J. 2019 Apr 11;32:180. [CrossRef] [PubMed]
3. Sangro P, Bilbao I, Fernández-Ros N, Iñarrairaegui M, Zulueta J, Bilbao JI, Sangro B. Pneumatocele during sorafenib therapy: first report of an unusual complication. Oncotarget. 2017 Dec 22;9(5):6652-6. [CrossRef] [PubMed]
4. Quigley MJ, Fraser RS. Pulmonary pneumatocele: pathology and pathogenesis. AJR Am J Roentgenol. 1988 Jun;150(6):1275-7. [CrossRef] [PubMed]
5. Zuhdi MK, Spear RM, Worthen HM, Peterson BM. Percutaneous catheter drainage of tension pneumatocele, secondarily infected pneumatocele, and lung abscess in children. Crit Care Med. 1996 Feb;24(2):330-3. [CrossRef] [PubMed]
6. Kaira K, Ishizuka T, Yanagitani N, Sunaga N, Hisada T, Mori M. Pulmonary traumatic pneumatocele and hematoma. Jpn J Radiol. 2009 Feb;27(2):100-2. [CrossRef] [PubMed]
7. Kesieme EB, Kesieme CN, Akpede GO, Okonta KE, Dongo AE, Gbolagade AM, Eluehike SU. Tension pneumatocele due to Enterobacter gergoviae pneumonia: a case report. Case Rep Med. 2012;2012:808630. [CrossRef] [PubMed]
8. Dines DE. Diagnostic significance of pneumatocele of the lung. JAMA. 1968 Jun 24;204(13):1169-72. [CrossRef] [PubMed]
9. Nayeemuddin M, Jankowich MD, Noska A, Gartman EJ. A strange case of coccidioidomycosis: utilization of bronchoscopy to diagnose a chronic cavitary lesion. Am J Resp Crit Care Med. 2018;197:A5427 [Abstract].

Cite as: Moses S, Gardner G, Starobinska E, Wolff A. Medical image of the month: coccidioidal pneumatocele complicated by pulmonary hemorrhage. Southwest J Pulm Crit Care. 2020;20(3):84-6. doi: https://doi.org/10.13175/swjpcc008-20 PDF 

Medical Image of the Month: Large Complex Cerebral Arteriovenous Malformation

Figure 1. Computed tomography angiography of the head showing the large complex arteriovenous malformation near the midline of the brain. A: sagittal plane the malformation is fed predominantly by the anterior circulation more on the right and the left. B: coronal plane.

A 70-year-old woman with a history of hypertension presented with left-sided weakness, headache, nausea, and vomiting. She denied loss of consciousness or seizure activity. On examination, she had receptive aphasia. Pupils were equal, round and reactive. She had neck pain on flexion. Her left upper extremity was plegic. Computed tomography of the brain showed acute hemorrhage involving the right thalamus, extending into the ventricular system, and a midline mass. She underwent a computed tomography angiogram, which showed a large, complex arteriovenous malformation (AVM) with a dilated branch of the right suprasellar internal carotid artery feeding the AVM, which then drained into the vein of Galen and straight sinus (Figure 1). She was monitored in the intensive care unit without worsening neurological deficit. She was discharged to a rehabilitation facility, having had no intravascular or surgical intervention.

AVMs are intracranial vascular anomalies which occur in 0.1% of the population (1). Clinical presentations include intracranial hemorrhage, seizures, headaches and neurological deficits, with hemorrhage being the most common and significant manifestation (2). The gold standard imaging modality is conventional cerebral angiography (1). Treating an AVM is a challenging clinical problem, as the risk of treatment has to be weighed against the natural history of the condition. Treatment modalities include observation with medical management, surgical resection, stereotactic radiosurgery, and endovascular embolization (1,2).

Vedhapriya Srinivasan MD, Piruthiviraj Natarajan MD, Reuben De Almeida, Safal Shetty MD, and Kulothungan Gunasekaran MD.

Bridgeport Hospital

Yale New Haven Health

New Haven, CT USA

References

1. Ajiboye N, Chalouhi N, Starke RM, Zanaty M, Bell R. Cerebral arteriovenous malformations: evaluation and management. ScientificWorldJournal 2014;2014:649036. [CrossRef] [PubMed]
2. Geibprasert S, Pongpech S, Jiarakongmun P, Shroff MM, Armstrong DC, Krings T. Radiologic assessment of brain arteriovenous malformations: what clinicians need to know. RadioGraphics. 2010;30:483-501. [CrossRef] [PubMed]

Cite as: Srinivasan V, Natarajan P, De Almeida R, Shetty S, Gunasekaran K. Medical image of the month: large complex cerebral arteriovenous malformation. Southwest J Pulm Crit Care. 2019;19(3):97-8. doi: https://doi.org/10.13175/swjpcc027-19 PDF 

Medical Image of the Week: Moyamoya Disease

Figure 1. Cerebral angiogram of the brain demonstrating bilateral high-grade stenosis of the anterior and middle cerebral arteries, worse on the left.

Figure 2. Magnetic resonance imaging showing multiple punctate infarcts in the frontal and parietal lobes on the left side.

A 52-year-old, right-handed, Caucasian woman with a history of hypertension and morbid obesity presented with acute onset of word-finding difficulty and slurred speech. Her medical and family history was negative for cerebral vascular event, coronary artery disease or smoking. Computed tomography of the patient's brain showed narrow caliber middle cerebral artery vasculature bilaterally. This abnormal finding prompted further investigation with cerebral angiogram. The angiogram showed bilateral high-grade stenosis of the anterior and middle cerebral arteries, worse on the left (Figure 1). Magnetic resonance imaging revealed multiple left sided punctate infarcts in the frontal and parietal lobes (Figure 2). Diagnosis of ischemic stroke secondary to moyamoya disease was established. This patient was not a candidate for fibrinolytic therapy since it had been more than 4 hours from initial presentation. She was treated with aspirin, clopidogrel, and atorvastatin for secondary prevention of ischemic stroke. Two months after her discharge date, the patient had a middle cerebral artery to superior temporal artery bypass on the left side, followed by a middle cerebral artery to superior temporal artery bypass on the right two months after initial bypass. Patient progressed to an uneventful recovery. Discharge planning included the continuation of aspirin, clopidogrel, and atorvastatin indefinitely.

Moyamoya disease (MMD) is an uncommon vasculopathy of unknown origin associated with diverse risk factors (1). It was first discovered in a Japanese population, and reported more commonly in this sub-population. However, numerous cases were reported across the globe (2). Moyamoya disease associated with other systemic condition such as neurofibromatosis type 1, trisomy 21, thyroid cranial irradiation or thyroid disease is termed moyamoya syndrome (MMS) (1,2). Moyamoya syndrome is a cerebrovasculopathy originating from collateral flow that develops secondary to occlusion of the internal carotid artery and the proximal afferent vessels at the circle of Willis (3). MMS can have abrupt or insidious onset and may progress to diversifying cerebral ischemic stroke or to intracranial hemorrhage, which is a worse prognosis and the primary cause of death in patients with MMD (4). It has been shown that ischemic stroke associated with MDD or MMS usually occurs when compensatory collateral vessels are unable to supply sufficient blood to the brain after occlusion or stenosis of the internal carotid arteries or its tributary vessels (5,6). On the other hand, intracranial hemorrhage occurs secondary to the rupture of abnormal moyamoya vessels (7,8).

It is imperative to differentiate between non-hemorrhagic and hemorrhagic moyamoya. Neuroimaging is the preferred method of diagnosis after high clinical suspicion of MMD or MMS. Intracranial hemorrhage and cerebral infarction can be diagnosed with computed tomography and magnetic resonance imaging/ cerebral angiogram, respectively (8,9). Recent use of magnetic resonance perfusion imaging has been shown to be crucial in diagnostics and medical-surgical decision making. There is no common consensus when it comes to treatment of moyamoya at this time. Initial management is symptomatic with anticoagulants, antiplatelet and corticosteroids (10). Treatment options may also include direct or indirect surgical revascularization as optimal therapy (11,12).

Stella Pak MD, Kokou Adompreh-Fia MD, Damian Valencia MD, Adam Fershko MD, and Jody Short DO.

Department of Medicine

Kettering Medical Center

Kettering, OH USA

References

1. Phi JH, Wang KC, Lee JY, Kim SK. Moyamoya Syndrome: A window of moyamoya disease. J Korean Neurosurg Soc. 2015 Jun;57(6):408-14. [CrossRef] [PubMed]
2. Suzuki J, Takaku A. Cerebrovascular "moyamoya" disease. Disease showing abnormal net-like vessels in base of brain. Arch Neurol. 1969 Mar;20(3):288-99. [CrossRef] [PubMed]
3. Yamamoto, S, Koh M, Kashiwazaki D, Akioka N, Kuwayama N, Noguchi K, Kuroda S. Is Quasi-moyamoya disease a uniform disease entity? A three-dimensional constructive interference in steady state imaging study. J Stroke Cerebrovasc Dis. 2016 Jun;25(6):1509-16. [CrossRef] [PubMed]
4. Baba, T., Houkin, K. Kuroda. Novel epidemiological features of moyamoya disease. J Neurol Neurosurg Psychiatry. 2008 Aug;79(8):900-4. [CrossRef] [PubMed]
5. Miyamoto S, Kikuchi H, Karasawa J, Nagata I, Ihara I, Yamagata S. Study of the posterior circulation in moyamoya disease. Part 2: Visual disturbances and surgical treatment. J Neurosurg. 1986 Oct;65(4):454-60. [CrossRef] [PubMed]
6. Kuroda S, Ishikawa T, Houkin K, Iwasaki Y. Clinical significance of posterior cerebral artery stenosis/occlusion in moyamoya disease. No Shinkei Geka. 2002 Dec;30(12):1295-300. [PubMed]
7. Kang K, Lu J, Zhang D, Li Y, Wang D, Liu P, Li B, Ju Y, Zhao X. Difference in cerebral circulation time between subtypes of moyamoya disease and moyamoya syndrome. Sci Rep. 2017;7(1):2587. [CrossRef] [PubMed]
8. Lui, P, Han C, Li DS, Lv XL, Li YX, Duan L. Hemorrhagic moyamoya disease in children: Clinical, angiographic features, and long-term surgical outcome. Stroke. 2016 Jan;47(1):240-3. [CrossRef] [PubMed]
9. Kellner CP, McDowell MM, Phan MQ, Connolly ES, Lavine SD, Meyers PM, Sahlein D, Solomon RA, Feldstein NA, Anderson RC. Number and location of draining veins in pediatric arteriovenous malformations: association with hemorrhage. J Neurosurg Pediatr. 2014 Nov;14(5):538-45. [CrossRef] [PubMed]
10. Whitaker J. Management of moyamoya syndrome [comment]. Arch Neurol. 2001;58:132. [CrossRef] [PubMed]
11. Golby AJ, Marks MP, Thompson RC, Steinberg GK. Direct and combined revascularization in pediatric moyamoya disease. Neurosurg. 1999;45:50-8. [PubMed]
12. Mizoi K, Kayama T, Yoshimoto T, Nagamine Y. Indirect revascularization for moyamoya disease: is there a beneficial effect for adult patients? Surg Neurol. 1996;45:541-8. [CrossRef] [PubMed] 

Cite as: Pak S, Adompreh-Fia K, Valencia D, Fershko A, Short J. Medical image of the week: moyamoya disease. Southwest J Pulm Crit Care. 2017;15(5):227-9. doi: https://doi.org/10.13175/swjpcc136-17 PDF

Medical Image of the Week: Chemotherapy-Induced Diffuse Alveolar Hemorrhage

Figure 1. Panel A: Chest X-ray on admission consistent showing some pulmonary edema and effusions at the bases. Panel B: Chest X-ray after initiation of chemotherapy showing diffuse bilateral infiltrates and consolidation.

Figure 2. CT scan of the chest after initiation of chemotherapy showing patchy ground glass consolidation throughout the lung fields bilaterally. Large bilateral pleural effusions can also be seen.

A 65-year-old man presented with relapse of his acute myeloid leukemia (AML). On admission he was seen to have a reduced ejection fraction at 40-50%. His chest X-ray showing pulmonary edema and bilateral pleural effusions (Figure 1A). He was diuresed to his dry weight to improve his clinical status. The decision was made to re-induce him for his AML with fludarabine and cytarabine without idarubicin (due to his reduced ejection fraction). After 2 doses of each the fludarabine and cytarabine the patient showed worsening respiratory distress, had increasing oxygen requirements and started having hemoptysis. Repeat imaging of his chest showed bilateral infiltrates in his lungs on both chest x-ray (Figure 1B) and chest CT (Figure 2). Infectious causes for the changes were sought and ruled out. He was transferred to the ICU where he was put on high flow oxygen and received methylprednisolone 1000 mg IV daily for 3 days. During this period his blood hemoglobin also dropped from 8.2 g/dl to 6.8 g/dl requiring transfusion of 1 unit of packed red blood cells. After 3 days of supportive care he was transferred back out of the ICU on oxygen by nasal cannula with progressive improvement in his lung function. Pulmonary toxicity is a known side effect resulting from both fludarabine and cytarabine and can present in a variety of forms. Their prompt recognition is important due to the steroid responsive nature of many of these once infectious causes have been ruled out.

Saud Khan, MD and Huzaifa A. Jaliawala, MD

Department of Internal Medicine

University of Oklahoma Health Sciences Center

Oklahoma City, OK USA

References

1. Helman DL Jr, Byrd JC, Ales NC, Shorr AF. Fludarabine-related pulmonary toxicity: a distinct clinical entity in chronic lymphoproliferative syndromes. Chest. 2002 Sep;122(3):785-90. [CrossRef] [PubMed]
2. Rudzianskiene M, Griniute R, Juozaityte E, Inciura A, Rudzianskas V, Emilia Kiavialaitis G. Corticosteroid-responsive pulmonary toxicity associated with fludarabine monophosphate: a case report. Turk J Haematol. 2012 Dec;29(4):392-6. [CrossRef] [PubMed]
3. Forghieri F, Luppi M, Morselli M, Potenza L.Cytarabine-related lung infiltrates on high resolution computerized tomography: a possible complication with benign outcome in leukemic patients. Haematologica. 2007 Sep;92(9):e85-90. [CrossRef] [PubMed]

Cite as: Khan S, Jaliawala HA. Medical image of the week: chemotherapy-induced diffuse alveolar hemorrhage. Southwest J Pulm Crit Care. 2017;15(5):219-20. doi: https://doi.org/10.13175/swjpcc131-17 PDF

Medical Image of the Week: Pulmonary Infarction- the “Reverse Halo Sign”

Figure 1. CT Chest with contrast. Two different levels in the same patient displayed on mediastinal windows. Several triangular shaped subpleural lesions with annular peripheral solid appearance are depicted, better characterized in the lung windows below (yellow arrows). Note the partial filling defect (red arrow on B), indicating a non-occlusive thrombus(arrow). Bilateral pleural effusions are also identified.

Figure 2. CT Chest with contrast, lung window corresponding to the levels in Figure 1 above. Note the triangular shaped subpleural lesions with peripheral solid appearance and ground glass center, characteristic of the atoll sign (arrows). As above, bilateral pleural effusions are present.

Pulmonary infarction is a known complication of pulmonary embolism (PE), a common disorder that results in 100,000-200,000 deaths annually in the United States. Computed tomography (CT) is the first-line modality to assess the pulmonary circulation with the ability to directly the visualize pulmonary emboli as well as pleuro-parenchymal abnormalities.

The appearance of a pulmonary infarct varies depending on the degree of ischemic injury in the setting of a dual blood supply to the lung. Infarcts occur more commonly in the periphery of the lung, given, the alternate blood supply by the bronchial arteries, is not as efficient as it is centrally. This location is also favored by the more common occurrence after occlusion of small peripheral arteries of 3 mm or less in caliber.

On CT lung infarcts can take the can take the “reverse halo” sign, also known as the “atoll” sign configuration, representing a focal area of decreased enhancement, and surrounding solid appearance. In the case of lung infarcts, the lesions typically have a broad pleural base triangular form with apex toward the hilum (1). Pathologically this corresponds to a hemorrhagic consolidation. The center of the lesion appears to correspond to aerated non-infarcted lung coexisting side by side with infarcted lung in the same lobule. The broad-based configuration is explained by the fan shaped distribution of the arteries as they extend out into the periphery. The convex border reflects the extravasated blood within the infarcted lung. Once the hemorrhage reabsorbs, the infarct heals completely or may leave behind a linear band of scarring.

From the imaging stand point, the reverse halo sign initially described in cryptogenic organizing pneumonia, has also been noted in patients with fungal disease, granulomatosis with polyangiitis, sarcoidosis and neoplastic disease among others (2).

George R Wu MS IV¹, Berndt Schmit MD², Veronica Arteaga MD², and Diana Palacio MD²

¹Arizona College of Osteopathic Medicine, Midwestern University, Glendale, AZ USA

²Division of Thoracic Imaging, University of Arizona, Tucson, AZ USA

References

1. He H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. J Thorac Imaging. 2006;21(1):1-7. [CrossRef] [PubMed]
2. Godoy MC, Viswanathan C, Marchiori E, et al. The reversed halo sign: update and differential diagnosis. Br J Radiol. 2012;85(1017):1226-35. [CrossRef] [PubMed]

Cite as: Wu GR, Schmit B, Arteaga V, Palacio D. Medical image of the week: pulmonary infarction- the “reverse halo sign”. Southwest J Pulm Crit Care. 2017;15(4):162-3. doi: https://doi.org/10.13175/swjpcc124-17 PDF 

Medical Image of the Week: Diffuse Axonal Injury

Figure 1. Panel A: Non-contrast CT of the head demonstrating hyperdense foci at the gray-white junction of the cortex and subcortical white matter (red arrows). Panel B: Hyperdense focus in the pons (red arrow).

Figure 2. MRI of the brain with a gradient recall echo (GRE) sequence demonstrating more pronounced hypointense foci consistent with hemorrhage.

An 18-year-old man without any significant past medical history presented to the emergency room trauma bay as an unrestrained passenger involved in a head-on collision at 85 mph. In the emergency room, he was found to have a GCS of 6 and was intubated for airway protection. A non-contrast CT of the head demonstrated hyperdense foci in the frontal lobes at the gray-white junction (Figure 1A) and a hyperdense focus in the pons (Figure 1B) consistent with punctate hemorrhages. An MRI of the brain with a gradient recall echo (GRE) sequence (Figure 2) demonstrated more pronounced hypointense foci consisent with hemorrhage. In the setting of the patient’s deceleration injury, the summation of his clinical and imaging findings was consistent with diffuse axonal injury.

Diffuse axonal injury (DAI) is pattern of closed head injury that results in a traumatic shear injury to the neuronal axons secondary to sudden deceleration and change in angular momentum. This pattern of injury often occurs at the interface between tissues of differing density such as the gray-white junction of the cerebral cortex and subcortical white matter. DAI can also be seen in deeper portions of the brain, such as the corpus callosum and brainstem, that are relatively fixed compared with more superficial portions of the brain resulting in greater rotational/ shear stress forces focused in these locations during sudden deceleration. Visible lesions on CT often underestimate the extent of neuronal injury (often described as the “tip of iceberg”), and neuronal injury is better delineated on MRI.

Most patients present with an immediate coma necessitating intubation for airway protection.  In mild cases, patients often experience mild traumatic brain injury characterized by heachaces, mild cognitive impairment, and personality changes. In more severe cases, DAI can result in a persistent vegetative state. Treatment is supportive in all cases.

Jack Hannallah, MD¹; Tammer Elaini, MD²; Kelly Wickstrom, DO³; Rorak Hooten, MD³; Michael Habib, MD²

Departments of ¹Surgery,²Pulmonary/Critical Care, and ³Internal Medicine

University of Arizona

Tucson, AZ USA

References

1. Yanagawa Y, Sakamoto T, Takasu A, Okada Y. Relationship between maximum intracranial pressure and traumatic lesions detected by T2*-weighted imaging in diffuse axonal injury. J Trauma. 2009;66(1):162-5. [CrossRef] [PubMed] 
2. Tong KA, Ashwal S, Holshouser BA, Shutter LA, Herigault G, Haacke EM, Kido DK. Hemorrhagic shearing lesions in children and adolescents with posttraumatic diffuse axonal injury: improved detection and initial results. Radiology. 2003;227(2):332-9. [CrossRef] [PubMed] 

Cite as: Hannallah J, Elaini T, Wickstrom K, Hooten R, Habib M. Medical image of the week: diffuse axonal injury. Southwest J Pulm Crit Care. 2015;11(6):264-5. doi: http://dx.doi.org/10.13175/swjpcc121-15 PDF

Medical Image of the Week: Abdominal Compartment Syndrome Due to Massive Upper Gastrointestinal Hemorrhage

Figure 1. Coronal section demonstrating a section of the Minnesota Tube within the stomach (yellow arrow), severe dilatation of the stomach (green arrow) and small bowel (blue arrow) due to intraluminal filling from blood. There is markedly reduced lungs volumes due to superior displacement of the diaphragm.

Figure 2. Saggital section demonstration the Minnesota Tube in place within the esophagus and stomach (yellow arrow) surrounded with intraluminal blood. There is intraluminal filling of the small intestine as well (green arrow).

A 29 year old woman with history of a Whipple procedure for pancreatic cancer and nonalcoholic steatohepatitis cirrhosis presented with a massive upper gastrointestinal bleeding (UGIB) likely from esophageal varices and developed hemorrhagic shock.

Emergent upper endoscopy could not be performed due to hemodynamic instability. Therefore, a Minnesota Tube was placed emergently for balloon tamponade of the bleeding. A transjugular intrahepatic portosystemic shunt was also placed emergently to decrease bleeding by reducing portal pressure. By this time, the patient had received 4 liters of normal saline, 14 units of packed red blood cells, 6 units of platelets, and 4 units of fresh frozen plasma.

The Minnesota tube did control the bleeding somewhat, however, there was continued bloody drainage from the stomach port of the Minnesota tube. The patient’s abdomen became remarkably distended and was dull to percussion throughout. A CT scan of the abdomen and pelvis revealed severe dilatation of the stomach and multiple loops of small bowel filled with mixed density blood (Figures 1 and 2). Intraabdominal bladder pressure was elevated to 34 mmHg. Given the radiographic findings, elevated bladder pressures, worsening lactic acid level and renal function, the patient was diagnosed with abdominal compartment syndrome. She was not a surgical candidate due to her grim prognosis. A large bore tube was placed into the abdominal cavity to drain ascitic fluid in effort to relieve the abdominal pressure.

Aggressive resuscitation including fluids, blood products, and four vasopressors was continued for the next several hours. However, due to patient’s poor prognosis, a decision was made to proceed with comfort care and the patient shortly passed away.

Acute upper gastrointestinal bleeding is a frequently encountered condition in the intensive care unit . Initial management generally consists of airway protection, intravascular resuscitation, correction of any coagulopathies, and acid-suppressive therapy (1). For UGIB with hemodynamic compromise, immediate upper endoscopic evaluation is indicated. The upper endoscopy allows for determination of the specific etiology of UGIB and for interventional therapy. If endoscopy cannot be done, bleeding cannot be controlled with endoscopic interventions or the patient is hemodynamically unstable, balloon tamponade should be considered (2). It is important to note that balloon tamponade is considered a bridge to more definitive therapy. Lastly, a multidisciplinary approach for management of massive UGIB should always be utilized especially in difficult cases.

VuAnh N. Truong, MD

Department of Medicine

Loma Linda University Medical Center

Loma Linda, CA

References

1. Conrad SA. Acute upper gastrointestinal bleeding in critically ill patients: causes and treatment modalities. Crit Care Med. 2002;30(6 Suppl):S365-8. [CrossRef] [PubMed]
2. Chen YI, Dorreen AP, Warshawsky PJ, Wyse JM. Sengstaken-Blakemore tube for non-variceal distal esophageal bleeding refractory to endoscopic treatment: a case report & review of the literature. Gastroenterol Rep (Oxf). 2014; Gastroenterol Rep (Oxf). 2014;2(4):313-5. [CrossRef] [PubMed] 

Reference as: Truong VN. Medical image of the week: abdominal compartment syndrome due to massive upper gastrointestinal hemorrhage. Southwest J Pulm Crit Care. 2014;9(5):284-6. doi: http://dx.doi.org/10.13175/swjpcc133-14 PDF

Medical Image of the Week: Massive Spontaneous Intra-Abdominal Bleeding

Figure 1. CT scan of the abdomen and pelvis showing diffuse intra-abdominal bleeding.

A 67 year-old female with RA, on anti-TNF and steroids, was admitted to the ICU with severe shock, likely hemorrhagic. She was on Coumadin for atrial fibrillation. She was found to have severe coagulopathy and diffuse spontaneous abdominal bleeding (Figure 1). She also developed left popliteal artery thrombosis, with compartment syndrome requiring surgical intervention. DIC was the final diagnosis.

Mohammed Alzoubaidi MD, Carmen Luraschi-Monjagatta MD, Sridhar Reddy MD, Robert McAtee MD.

Departments of Pulmonary and Critical Care, Internal Medicine and Emergency Medicine

South Campus

Tucson, Arizona

Reference as: Alzoubaidi M, Luraschi-Monjagatta C, Reddy S, McAtee R. Medical image of the week: massive spontaneous intra-abdominal bleeding. Southwest J Pulm Crit Care. 2014;8(2):135. doi: http://dx.doi.org/10.13175/swjpcc018-14 PDF