Medical Image of the Month: Glioblastoma Multiforme

Figure 1. Non-contrast CT axial views of what was later identified as glioblastoma multiforme demonstrates heterogeneous left frontal lobe mass with foci of hemorrhage (black arrows, A), mass effect (gray arrow, A & B), central necrosis (gray arrowhead, C), invasion of the corpus callosum (gray arrowhead, C), and vasogenic edema (white arrow, D).

A patient in their 60's presented with headaches for approximately 2 weeks followed by acutely worsening mental status with confusion. CT of the head is shown (Figure 1). Glioblastoma multiforme was high on the differential diagnosis.

Glioblastoma multiforme (GBM) is classified as a grade IV astrocytoma and is the most common malignant primary brain tumor. It has an incidence of 3.19 cases per 100,000 persons per year. Astrocytomas are the most invasive type of glial tumor, directly reflecting the remarkably poor prognosis with a 5-year survival rate of approximately 4% and a 26-33% survival rate at 2 years in clinical trials. Symptoms develop relatively rapidly due to edema and mass effect of the tumor. Increased intracranial pressure and swelling manifests as nausea, vomiting, seizures and headaches that are typically worse in the morning. Neurological symptoms are dependent on the location of the cerebrum that is affected (ex. sensory, motor, visual changes, gait disturbances). Conventional gadolinium-enhanced MR imaging is the standard technique for the evaluation of GBM. GBM is characterized by a large, heterogeneous mass in the cerebral hemisphere exhibiting hemorrhage, necrosis and enhancement. In addition, magnetic resonance tomography (MRS) and positron emission tomography (PET) can be used to examine the chemical profile and assist in detecting tumor recurrence, respectively. The current gold standard treatment for GBM is temozolomide in combination with radiation therapy. Two potential new treatment modalities currently under investigation are gene therapy and immunotherapy.

Biopsy of the patient’s mass confirmed glioblastoma multiforme, which was successfully treated without recurrence on MRI 18 months later.

Cassandra Ann Roose and Michael Craig Larson MD, PhD

Medical Imaging Department

Banner University Medical Center/University of Arizona

Tucson, AZ UA

References

1. Stoyanov GS, Dzhenkov DL. On the Concepts and History of Glioblastoma Multiforme - Morphology, Genetics and Epigenetics. Folia Med (Plovdiv). 2018;60(1):48-66. [CrossRef] [PubMed]
2. Altman DA, Atkinson DS Jr, Brat DJ. Best cases from the AFIP: glioblastoma multiforme. Radiographics. 2007;27(3):883-888. [CrossRef] [PubMed]
3. American Association of Neurological Surgeons. Glioblastoma Multiforme. Available from: https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Glioblastoma-Multiforme (accessed 8/24/20).

Cite as: Roose CA, Larson MC. Medical image of the month: glioblastoma multiforme. Southwest J Pulm Crit Care. 2020;21(3):64-5. doi: https://doi.org/10.13175/swjpcc046-20 PDF 

Medical Image of the Month: Renal Cell Carcinoma with Extensive Tumor Thrombus

Figure 1. CT of the abdomen with contrast (axial image) shows a large right large heterogeneous mass (red arrow), consistent with renal cell carcinoma.

Figure 2. A: CT of the abdomen with contrast (coronal image) shows a large right renal mass (green arrow) and tumor thrombus in the IVC (orange arrow). B: Sagittal image showing extension of the tumor thrombus from the inferior vena cava into the right atrium (blue arrow). C: Axial image showing evidence of tumor thrombus in the right atrium (pink arrow).

A 53-year-old man with a right-sided renal cell carcinoma (RCC) presented with nausea, vomiting, intolerance of oral intake and melena. A contrast enhanced CT of the abdomen and pelvis showed near complete replacement of the right kidney by a large heterogeneous mass, measuring 10 x 16 cm (Figure 1). The mass invaded the renal vein and inferior vena cava (IVC) with extension to the level of the inferior cavo-atrial junction (Figure 2). The mass compressed the duodenum, causing a bowel obstruction. Liver and lung metastases were also found. A duodenal stent was placed with significant improvement in his nausea and vomiting. He was not able to receive anticoagulation due to severe gastrointestinal bleeding. The patient discontinued disease modifying therapy and died four weeks after discharge from the hospital.

Tumor thrombus occurs when a tumor invades a blood vessel. It occurs in approximately 10% of patients with renal cell carcinoma, which is a highly vascular malignancy with a propensity to invade the venous system (1). Extension of the tumor from the inferior vena cava into the right atrium is very uncommon, seen in only about 1% of RCCs (1). The American Joint Committee on Cancer staging system for RCC differentiates between tumor thrombus involving the renal vein (T3a), IVC below the diaphragm (T3b) and IVC above the diaphragm (T3c) (1). The presence of tumor thrombus changes staging, prognosis and surgical options. Surgical treatment may be the approach to tumor thrombus in RCC without metastatic disease. The surgical approach is often complex and requires extensive surgical planning and expertise (2). Perioperative morbidity and mortality appear to be proportional to the height of tumor growth, and tumor thrombus extending above the diaphragm carries increased perioperative risk. Wagner et al. (3) retrospectively studied 1,192 cases, and found reduced long-term survival in patients with any venous involvement. However, they found no significant difference in long-term survival between patients with IVC tumor thrombus below (T3b) or above (T3c) the diaphragm. In this study, the most important prognostic factors in RCC included renal tumor size, the presence of perinephric fat invasion, lymph node involvement and distant metastatic lesions.

David Horn MD, Sue Cassidy ANP-BC and Linda Snyder MD

Departments of Internal Medicine and Pulmonary, Critical Care, Allergy and Sleep Medicine

University of Arizona College of Medicine

Tucson, AZ USA

References

1. Wotkowicz C, Wszolek MF, Libertino JA. Resection of renal tumors invading the vena cava. Urol Clin N Am. 2008; 35: 657-71. [CrossRef] [PubMed]
2. Quencer KB, Friedman T, Sheth R, Rahmi O. Tumor thrombus: incidence, imaging, prognosis and treatment. Cardiovasc Diagn Ther. 2017;7(Suppl 3):S165-77. [CrossRef] [PubMed]
3. Wagner B, Patard JJ, Méjean A, et al. Prognostic value of renal vein and inferior vena cava involvement in renal cell carcinoma. Eur Urol. 2009;55:452-9. [CrossRef] [PubMed]

Cite as: Horn D, Cassidy S, Snyder L. Medical image of the month: renal cell carcinoma with extensive tumor thrombus. Southwest J Pulm Crit Care. 2019;19(3):95-6. doi: https://doi.org/10.13175/swjpcc031-19 PDF 

Medical Image of the Month: Bilateral Atrial Enlargement

Figure 1. Portable chest radiograph showing elevation of the left mainstem bronchus (red arrow).

Figure 2. Thoracic CT scan showing right atrial enlargement (blue circle) and left atrium (red circle).

Figure 3. Upper Image: Static image from echocardiogram showing right atrial enlargement (white circle). Lower image: video of echocardiogram.

A 97-year-old woman was repeatedly admitted for dyspnea, hypoxemia and treated with antibiotics for presumed left lower lobe pneumonia. She has a past medical history of atrial fibrillation, congestive heart failure and sick sinus syndrome with placement of a cardiac pacemaker. Notably on physical examination, she had heart rate of 110 beats/minute, temperature of 98.8°F, blood pressure of 122/72 mm Hg, and a respiratory rate of 27 breaths/minute. She had a sternal heave, a grade 4/6 "blowing" holosystolic murmur, a loud S2, jugular venous distension and an enlarged liver. Chest x-ray showed obscuration of the left lower lobe - the left heart border cannot be seen, and the L mainstem bronchus is straightened and lifted superiorly (Figure 1). An image of the heart is shown from a CT abdomen obtained 6 months previously, showing cardiomegaly, particularly massive atrial enlargement (Figure 2). An ultrasound showed bilateral atrial enlargement with moderate mitral regurgitation and severe tricuspid regurgitation (Figure 3). The left ventricular ejection fraction was 55%, but with abnormal septal motion. She was treated with gentle diuresis to help relieve volume overload, and isosorbide dinitrate for preload and afterload reduction. Pulmonary hypertension was attributed to chronic mitral regurgitation. The cause was unclear - the patient remembered that her brother had rheumatic fever as a young recruit in WWII, but didn't know whether she had ever experienced it.

Atrial enlargement can be of prognostic significance. Left atrium size has been found to be a predictor of mortality due to both cardiovascular issues as well as all-cause mortality (1). Larger right atrium than left atrium has been associated with all-cause mortality in elderly patients with heart failure (2).

Robert A. Raschke, MD

University of Arizona College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Patel DA, Lavie CJ, Milani RV, Shah S, Gilliland Y. Clinical implications of left atrial enlargement: a review. Ochsner J. 2009 Winter;9(4):191-6. [PubMed]
2. Almodares Q, Wallentin Guron C, Thurin A, Fu M, Kontogeorgos S, Thunstrom E, Johansson MC. Larger right atrium than left atrium is associated with all-cause mortality in elderly patients with heart failure. Echocardiography. 2017 May;34(5):662-7. [CrossRef] [PubMed]

Cite as: Raschke RA. Medical image of the month: bilateral atrial enlargement. Southwest J Pulm Crit Care. 2019;19(1):10-1. doi: https://doi.org/10.13175/swjpcc023-19 PDF

Medical Image of the Month: Malignant Pleural and Pericardial Effusions

Figure 1. CTA chest axial view showing moderate pericardial effusion, bilateral pleural effusions and an anterior mediastinal mass.

Figure 2. Echocardiography subcostal four-chambered view showing a large pericardial effusion with right ventricular collapse during diastole.

A 67-year-old woman with a history of presumed thymoma presented to the emergency department with four weeks of progressive shortness of breath and wheezing. CT imaging of the chest on arrival demonstrated a 13.1 x 8.6 x 8.2 cm anterior mediastinal mass with compression of the SVC, pulmonary veins, and right pulmonary artery (Figure 1). A moderate pericardial effusion was also seen. A transthoracic echocardiogram was performed to further evaluate the pericardial effusion, which revealed diastolic collapse of the right ventricle consistent with cardiac tamponade (Figure 2). The patient was taken for urgent pericardiocentesis, which drained 450cc of sanguineous fluid. Percutaneous biopsy of the mass revealed poorly differentiated carcinoma suspicious for a primary breast malignancy. Cytology of the pericardial fluid did not demonstrate malignancy, however. Cytology of subsequent pleural effusion also was not positive for malignancy, although, both effusions are believed to be related to the malignancy even if no malignant cells were present on analysis.

Malignant pericardial effusions account for 18-23% of cases, and are one of the most common causes of hemorrhagic effusions. Multiple types of cancers can involve the pericardium; lung cancer is the most common but lymphoma, leukemia, melanoma, and breast cancer are other potentially causative malignancies. Presence of a symptomatic malignant effusion is a poor prognostic indicator with median survival on the order of 2-4 months after diagnosis, although certain malignancies (e.g. hematologic rather than solid) may have better results (1).

Nathan Coffman MD and Jessica Vondrak MD

Department of Internal Medicine

Banner University Medical Center

University of Arizona

Tucson, AZ USA

Reference

1. Dequanter D, Lothaire P, Berghmans T, Sculier JP. Severe pericardial effusion in patients with concurrent malignancy: a retrospective analysis of prognostic factors influencing survival. Ann Surg Oncol. 2008 Nov;15(11):3268-71. [CrossRef] [PubMed] 

Cite as: Coffman N, Vondrak J. Medical image of the month: Malignant pleural and pericardial effusions. Southwest J Pulm Crit Care. 2018;17(5): . doi: https://doi.org/10.13175/swjpcc107-18 PDF 

Medical Image of the Month: Superior Vena Cava Syndrome

Figure 1. Coronal CT thorax with contrast showing a large apical mass with near complete atelectasis of the right upper lobe, mediastinal extension and effacement of the superior vena cava (arrow).

Figure 2. Caval-superficial-umbilical-portal pathway.  EMV = external mammary vein, EV = epigastric vein, IEV = inferior epigastric vein, IMV = internal mammary vein, SEV= superior epigastric vein (2).

Figure 3. Axial CT thorax with contrast showing avid arterial enhancement of hepatic segment IV (arrow, hot quadrate sign), consistent with superior vena cava syndrome.

Although superior vena cava syndrome (SVCS) may result from internal or external occlusion of the superior vena cava, 60-90% of cases are caused by external compression from malignant tumors, predominately lung cancer and lymphoma (1). Additional causes of SVCS via external occlusion include fibrosing mediastinitis, while internal occlusion may result from pacemaker lead or indwelling central venous catheter thrombosis (1). Symptoms of SVCS, such as facial and neck swelling, dyspnea and cough, typically develop over 2-4 weeks prior to diagnosis, during which collateral vessels develop (2). More severe symptoms of disease include laryngeal edema, cerebral edema, orthostatic syncope secondary to decreased venous return and altered mental status (3). In the presence of SVCS, cavoportal collaterals that may develop include caval-superficial-umbilical-portal pathways and caval-mammary-phrenic-hepatic capsule-portal pathways (3). Figure 2 demonstrates the anastomosis of inferior and superficial epigastric veins with internal and external mammary veins, allowing for recanalization of the paraumbilical vein and drainage into left portal vein. The presence of a caval-superficial-umbilical-portal pathway may be detected as a wedge-shaped area of increased enhancement in segment IV of the liver on CT or MRI, a radiographic finding known as the hot quadrate sign (Figure 3). Following diagnosis of SVCS in the setting of malignancy, goals of management may be palliative or curative and should take into account life expectancy. Endovascular stenting can provide near immediate symptomatic relief of SVCS, but requires the addition of chemotherapy, radiotherapy or combined-therapy if the goals of treatment are curative (1). Although the median life expectancy of a patient with SVCS due to underlying malignancy is often reported as 6 months, the prognosis is dependent on tumor type and the presence or absence of poor prognostic factors, including age >50 years old, history of tobacco use and treatment with corticosteroids (3).

Elliot Breshears MS IV, Lev Korovin MD, and Veronica Arteaga MD.

Department of Medical Imaging

The University of Arizona

Tucson, AZ, USA

References

1. Wan JF, Bezjak A. Superior vena cava syndrome. Hematol Oncol Clin North Am. 2010;24(3):501-13. [CrossRef] [PubMed]
2. Kapur S, Paik E, Rezaei A, Vu DN. Where there is blood, there is a way: unusual collateral vessels in superior and inferior vena cava obstruction. RadioGraphics. 2010;30(1):67-78. [CrossRef] [PubMed]
3. Manthey DE, Ellis LR. Superior vena cava syndrome (SVCS). In: Todd KH, Thomas CR Jr. Oncologic Emergency Medicine: Principles and Practice. Switzerland: Springer; 2016:211-222. Available at: https://books.google.com/books?id=_qQqDAAAQBAJ&pg=PA211&lpg=PA211&dq=Manthey+DE,+Ellis+LR.&source=bl&ots=MWH6bcbHSf&sig=L7Ul5sfS1sSGBTF5cnK7MvKF9eA&hl=en&sa=X&ved=2ahUKEwjGkoTC9LrdAhUEEHwKHbV2CF4Q6AEwAHoECAEQAQ#v=onepage&q=Manthey%20DE%2C%20Ellis%20LR.&f=false (accessed 9/14/18).

Cite as: Breshears E, Korovin L, Arteaga V. Medical image of the month: superior vena cava syndrome. Southwest J Pulm Crit Care. 2018;17(4):114-5. doi: https://doi.org/10.13175/swjpcc103-18 PDF 

Medial Image of the Week: Purpura Fulminans

Figure 1.  A: Purpura fulminans. B: Close up view of the left lower extremity.

A 54-year-old man with coronary artery disease, fibromyalgia and chronic sacral ulcers was brought to the emergency department due to acute changes in mentation and hypotension. He suffered a cardiac arrest shortly after arrival to the emergency department during emergent airway management. After successful resuscitation, he was admitted to the medical intensive care unit and treated for septic shock with fluid resuscitation, vasopressors and broad spectrum antibiotics. Laboratory results were significant for disseminated intravascular coagulopathy (DIC)- thrombocytopenia, decreased fibrinogen and elevated PT, PTT and D-dimer levels. Profound metabolic acidosis and lactate elevation was also seen. Blood Cultures later revealed a multi-drug resistant E. coli bacteremia. Images of the lower extremities (Figure 1) were obtained at initial assessment and are consistent with purpura fulminans. He did not survive the stay.

Purpura fulminans, also referred to as skin mottling, is an evolving skin condition which is characterized by an acutely worsening reticular pattern of ecchymosis, tissue thrombosis and eventual hemorrhagic skin necrosis. Traditionally associated with either an inherited and/or acquired protein C deficiency, it is more commonly seen in DIC. It is generally considered a poor prognostic indicator when associated with DIC. In our patient, the DIC was secondary to septic shock. When encountered in this clinical scenario it should be considered an acute life threatening emergency.

Emilio Perez Power MD¹, Norman Beatty MD¹ and Bhupinder Natt MD²

¹Department of Internal Medicine and ²Division of Pulmonary, Allergy, Critical Care and Sleep

Banner-University Medical Center South Campus

University of Arizona

Tucson, AZ USA

Cite as: Power EP, Beatty N, Natt B. Medical image of the week: purpura fulminans. Southwest J Pulm Crit Care. 2016;13(6):307-8. doi: https://doi.org/10.13175/swjpcc129-16 PDF

Medical Image of the Week: Pulsus Alternans

Figure 1. Telemetry display including arterial pressure waveform, which demonstrates alternating beats of large (large arrows) and small (small arrows) pulse pressure. Concurrent pulse oximetry could not be performed at the time of the image due to poor peripheral perfusion.

A 52 year old man with a known past medical history of morbid obesity (BMI, 54.6 kg/m²), heart failure with preserved ejection fraction, hypertension, untreated obstructive sleep apnea, and obesity hypoventilation syndrome presented with increasing dyspnea over several months accompanied by orthopnea and weight gain that the patient had treated at home with a borrowed oxygen concentrator. On arrival to the Emergency Department, the patient was in moderate respiratory distress and hypoxic to SpO2 70% on room air. Physical examination was pertinent for pitting edema to the level of the chest. Assessment of jugular venous pressure and heart and lung auscultation were limited by body habitus, but chest radiography suggested pulmonary edema. The patient refused aggressive medical care beyond supplemental oxygen and diuretic therapy. Initial transthoracic echocardiography was limited due to poor acoustic windows but suggested a newly depressed left ventricular ejection fraction (LVEF) of <25%. The cause, though uncertain, may have been reported recent amphetamine use. The patient deteriorated, developing shock and respiratory failure; after agreeing to maximal measures, ventilatory and inotropic/vasopressor support was initiated.

Shortly after placement of the arterial catheter, the ICU team was called to the bedside for a change in the arterial pressure waveform (Figure 1), which then demonstrated alternating strong (arrow) and weak beats (arrow head) independent of the respiratory cycle. The waveform was recognized as pulsus alternans. Repeat bedside echocardiography suggested severe biventricular systolic impairment and LVEF of approximately 5-10%, later confirmed by formal transesophageal ehocardiography performed prior to a cardioversion for atrial flutter.

Pulsus alternans was first formally described in 1872 and associated with severe left ventricular systolic dysfunction (1). The pattern of pulsus alternans is detectable by palpation, arterial pressure waveform analysis, and Doppler echocardiography. Competing theories in the early 20^th century attempted to explain this finding. Wenkebach and Straub, using the Starling relationship, suggested that the alternating force of the pulse is due to alternating filling volumes: greater diastolic volumes accommodated by increased fiber length caused forceful contraction/greater stroke volume with subsequently reduced end systolic and therefore end diastolic volumes for the next (weaker) beat; the consequently reduced force left again greater end systolic and end diastolic volumes for the next (more powerful) beat thereafter. Gaskell, Hering, and Wiggers alternatively proposed the phenomenon was rooted in myocardial contractility fluctuations independent of volumes. Laboratory and animal data supported both theories, but seminal clinical work in the 1960s using concurrent ventriculography and ventricular pressure measurements demonstrated that both mechanisms, in fact, occur in different human subjects (2). The second, Starling-independent mechanism is now thought to be due at least in part to delayed intracellular calcium cycling leading to rhythmic fluctuations in excitation-contraction coupling (3).

Regardless of the underlying physiology, the significance of pulsus alternans as a harbinger of severe ventricular dysfunction and poor prognosis has been recognized and unquestioned since its description. This was unfortunately true in the case of our patient, who developed multiorgan failure despite resuscitative efforts and died three days after admission.

Luke M. Gabe, MD

University of Arizona College of Medicine

Department of Internal Medicine

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine

1501 N. Campbell Ave.

Tucson, AZ USA

References

1. Traube L. Ein fall von pulsus bigeminus nebst bemerkungen tiber die lebershwellungen bei Klappenfehlern und über acute leberatrophic. Ber Klin Wschr. 1872;9:185.
2. Cohn KE, Sandler H, Hancock EW. Mechanisms of pulsus alternans. Circulation. 1967 Sep;36(3):372-80. [CrossRef] [PubMed]
3. Euler DE. Cardiac alternans: mechanisms and pathophysiological significance. Cardiovasc Res. 1999 Jun;42(3):583-90. [CrossRef] [PubMed]

Cite as: Gabe LM. Medical image of the week: pulsus alternans. Southwest J Pulm Crit Care. 2016;13(5):266-7. doi: https://doi.org/10.13175/swjpcc123-16 PDF 

Medical Image of the Week: Intraventricular Hemorrhage Casting

Figure 1. Panel A: Computerized tomography of the head without contrast taken at an outlying facility displayed a right thalamic intraparenchymal hematoma, measuring 3.4 x 4.2 cm, with vasogenic edema and intraventricular rupture (blue arrow). Intraventricular hemorrhage casting is visualized in the right lateral ventricular causing obstructive hydrocephalus (red arrow). Panel B: Repeat non-contrast CT of the head 6 hours later revealed an increase in size of thalamic hematoma to 4.3 x 5.2 x 4.8 cm, an increase in amount of Intraventricular hemorrhage, progression of hydrocephalus from cast obstruction, and worsening vasogenic edema causing 5 mm left midline shift.

An 80-year-old woman with a past medical history of hypertension and hypercholesterolemia presented to an outlying hospital at 11:00 hours with slurred speech, left arm drift, and headache. A non-contrast CT of the head revealed an intraparenchymal hematoma in the right thalamus measuring 3.4 x 4.2 cm with an associated intraventricular rupture (Figure 1A, blue arrow). An intraventricular hemorrhage cast with secondary hydrocephalus was also noted on initial imaging (Figure 1A, red arrow). She was placed on a nicardipine drip for blood pressure control and subsequently transferred to OSF St. Francis Medical Center (OSFMC) for a higher level of care.

Upon arrival to OSFMC, the patient was poorly responsive, non-verbal, and could not follow commands.  She was directly admitted to the Neuroscience Intensive Care Unit for further management. Vitals signs were stable on presentation. Neurologic examination revealed a comatose patient with asymmetric and minimally reactive pupils, absent gag reflex, right gaze preference, brisk corneal reflex on the right and absent response on the left, absent deep tendon reflexes on the left upper and lower extremity, with absent response to painful stimuli on the left upper and lower extremity. Patient had a Glasgow Coma Scale score of 6, NIH stroke scale score of 23, and an Intracerebral Hemorrhage Score of 5. A repeat non-contrast CT scan of the head was performed at 17:00 hours to monitor for expansion of hematoma and progression of secondary hydrocephalus. Imaging revealed an interval increase in the size of the acute intraparenchymal hematoma, measuring 4.3 x 5.2 x 4.8 cm. In addition, there was an increase in amount of intraventricular hemorrhage, progression of hydrocephalus, and worsening vasogenic edema causing a mass effect with a 5 mm left midline shift (Figure 1B). At the request of the patient’s family members, her code status changed to DNR and she was made comfort care. No interventions were pursued and patient entered hospice care. 

Intracerebral hemorrhage (ICH) occurs in about 15% of strokes per year (1). The most common cause of spontaneous ICH is rupture of micro-aneurysms of small blood vessels in brain tissue, secondary to chronic hypertension. Hypertensive hemorrhages typically occur in the basal ganglia and thalamus, which are in close proximity to the cerebral ventricular system. Blood can accumulate at these sites forming an acute intraparenchymal hematoma, which can expand and exert mechanical pressure on the ventricular walls leading to intraventricular rupture and secondary intraventricular hemorrhage (IVH) (2). Intraventricular rupture occurs in approximately 45% of spontaneous ICH, which results in an expected mortality of 50-80% (1). Blood in the ventricular system can clot forming a “cast” (Figure 1A, red arrow). Ventricular casts are especially troublesome because the cast can block the outflow of cerebrospinal fluid causing an acute obstructive hydrocephalus, which can lead to increased intracerebral pressure (ICP), mass effect, and brain herniation (2). In Figure 1A, the intraventricular cast formation likely represents the patient’s normal ventricular size prior to ventriculomegaly from hydrocephalus. Figure 1B shows the typical progression of the intraparenchymal hematoma and obstructive hydrocephalus. There are several treatment options for management of an intraparenchymal hematoma with intraventricular rupture; they include reduction of ICP via ventriculostomy and medical therapy, surgical evacuation of the hematoma, and intraventricular thrombolytics to reduce casting and secondary obstructive hydrocephalus (2,3). Despite these interventions, the prognosis remains poor (3).

Melvin Parasram MS OMS4,¹ Mangala Gopal OMS4,² Lee Raube DO MS,³ Editha Johnson DO,⁴ Deepak Nair MD^4,5

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

²Des Moines University, College of Osteopathic Medicine, Des Moines, IA USA

³Departments of Emergency Medicine and ⁴Neurology, University of Illinois College of Medicine at Peoria, Peoria, IL USA  

⁵Illinois Neurological Institute, OSF St. Francis Medical Center, Peoria, IL USA

References

1. Hinson HE, Hanley DF, Ziai WC. Management of intraventricular hemorrhage. Curr Neurol Neurosci Rep. 2010 Mar;10(2):73-82. [CrossRef] [PubMed]
2. Hanley DF. Intraventricular hemorrhage: severity factor and treatment target in spontaneous intracerebral hemorrhage. Stroke. 2009 Apr;40(4):1533-8. [CrossRef] [PubMed]
3. Nieuwkamp DJ, de Gans K, Rinkel GJ, Algra A. Treatment and outcome of severe intraventricular extension in patients with subarachnoid or intracerebral hemorrhage: a systematic review of the literature. J Neurol. 2000 Feb;247(2):117-21. [CrossRef] [PubMed] 

Cite as: Parasram M, Gopal M, Raube L, Johnson E, Nair D. Medical image of the week: intraventricular hemorrhage casting. Southwest J Pulm Crit Care. 2016;13(5):220-3. doi: http://dx.doi.org/10.13175/swjpcc094-16 PDF 

Medical Image of the Week: Superior Vena Cava Syndrome

Figure 1. Contrast-enhanced CT of the chest in the arterial phase in the coronal plane demonstrates a large paratracheal mass (blue circle) that is invading the SVC resulting in the tumor thrombus noted in right heart chambers.

Figure 2. Contrast-enhanced CT of the chest in the arterial phase at the level of the right atrium (blue arrow), tricuspid annulus (yellow arrow), and right ventricle (green arrow) demonstrates a thrombus extending from the right atrium across the tricuspid valve in to the right ventricle.

A 65 year old Native American man with past medical history significant for hypertension presented with a two week history of generalized edema, most prominent in the face and upper extremities. The patient had gained 30 lbs in the previous 6 months. He denied any fever, night sweats, dyspnea, hemoptysis, change in voice, chest pain, abdominal pain, nausea, vomiting, or hematemesis but did acknowledge a 40+ pack-year smoking history. Family history was significant for two brothers deceased from lung cancer. On presentation, he was hemodynamically stable, had visibly distended neck veins and collateral veins on the chest and abdomen. Routine laboratory tests included a comprehensive metabolic panel remarkable for mild transaminitis, complete blood count with thrombocytopenia (69,000) and mild anemia (hemoglobin 13.5).  Urinalysis and infectious workup were unremarkable. A CT chest/abdomen/pelvis confirmed superior vena cava (SVC) syndrome from a thrombus in the right atrium extending cephalad into the SVC and left brachiocephalic vein. Patient was started on dexamethasone 4mg every 6 hours and a heparin drip. A fine needle biopsy of the large mediastinal paratracheal mass showed non-small cell lung carcinoma.  He received cycle 1 of carboplatin and docetaxel. Five days after chemotherapy, patient had large volume hemoptysis. Repeat CTA chest demonstrated enlargement of the right suprahilar mass invading the mediastinum/SVC with extension into the right atrium and crossing into the right ventricle (Image 1 and 2). Considering severity of the disease and poor prognosis patient and patient’s family accepted comfort care.

SVC syndrome results from mechanical obstruction of the SVC. Dyspnea, facial swelling and distended neck veins are the characteristic clinical manifestations (1). In the era of antibiotics, 70-90% of cases are due to mediastinal malignancies (2). Symptomatic relief with steroids, radiation/chemotherapy and intravascular stents are mainstays of emergent treatment (1). However, similar to our case, due to aggressive nature of the disease the mortality is inevitable.

Manjinder Kaur DO, Charity Adusei MS III, Tammer Elaini MD, and Laura Meinke MD

Department of Medicine

The University of Arizona and Sourthern Arizona VA Health Care System

Tucson, AZ, USA

References

1. Khan UA, Shanholtz CB, McCurdy MT. Oncologic mechanical emergencies. Emerg Med Clin North Am. 2014;32(3):495-508. [CrossRef] [PubMed]
2. Rossow CF, Luks AM. A 68-year-old woman with hoarseness and upper airway edema. Ann Am Thorac Soc. 2014;11(4):668-70. [CrossRef] [PubMed]

Cite as: Kaur M, Adusei C, Elaini T, Meinke L. Medical image of the week: superior vena cava syndrome. Southwest J Pulm Crit Care. 2015;11(3):114-5. doi: http://dx.doi.org/10.13175/swjpcc084-15 PDF

Medical Image of the Week: Panlobular Emphysema

Figure 1. PA chest radiograph showing predominately lower lobe emphysematous changes.

A 60 year old female, non-smoker with a past medical history of chronic rhinosinusitis with nasal polyps presented with an eight year history of productive cough and dyspnea. Previous treatment with inhaled corticosteroids, courses of systemic corticosteroids and antibiotics provided modest improvement in her symptoms. Pulmonary function testing revealed a severe obstructive ventilatory defect without significant bronchodilator response and reduced diffusing capacity (DLCO). Chest x-ray surprisingly revealed lower lobe predominant emphysematous changes (Figure 1). Alpha-1-antitrypsin level was within normal range at 137 mg/dL.

Panlobular emphysema represents permanent destruction of the entire acinus distal to the respiratory bronchioles and is more likely to affect the lower lobes compared to centrilobular emphysema (1). Panlobular emphysema is associated with alpha-1-antitrypsin deficiency, intravenous drug abuse specifically with methylphenidate and methadone, Swyer-James syndrome, and obliterative bronchiolitis. Whether this pattern is seen as part of normal senescence in non-smoking individuals remains controversial (2). Panlobular emphysema may represent a phenotypically more severe disease than centrilobular emphysema and may coexist along a continuum with centrilobular emphysema (3).

Ashish Mathur MD and Tara Carr MD

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine

University of Arizona College of Medicine

Tucson, Arizona

References

1. Litmanovich D, Boiselle PM, Bankier AA. CT of pulmonary emphysema-current status, challenges, and future directions. Eur Radiol. 2009;19(3): 537-51. [CrossRef] [PubMed]
2. Takahashi M, Fukuoka J, Nitta N et al. Imaging of pulmonary emphysema: a pictorial review. Int J Chron Obstruct Pulmon Dis. 2008;3(2):193-204. [PubMed]
3. Finkelstein R, Ma HD, Ghezzo H, Whittaker K, Fraser RS, Cosio MG. Morphometry of small airways in smokers and its relationship to emphysema type and hyperresponsiveness. Am J Respir Crit Care Med. 1995;152(1):267-76. [CrossRef] [PubMed]

Reference as: Mathur A, Carr T. Medical image of the week: panloubular emphysema. Southwest J Pulm Criti Care. 2015;11(2):86-7. doi: http://dx.doi.org/10.13175/swjpcc081-15 PDF

Medical Image of the Week: Cheyne-Stokes Respiration

Figure 1. Cheyne-Stokes Breathing pattern seen. The red arrow indicates the cycle time which is defined as the duration of the central apnea (or hypopnea) + the duration of a respiratory phase.

A 62 year-old male with a past medical history congestive heart failure, chronic obstructive pulmonary disease, and obesity with a body mass index of 38.02 kg/m² underwent an overnight polysomnogram for clinical suspicion for obstructive sleep apnea. He was found to have a periodic breathing as seen in the image above.

Cheyne-stokes respiration (CSR) is a type of periodic breathing characterized by crescendo-decrescendo pattern of respiration separated by central sleep apneas (CSA) or hypopneas (1). CSR-CSA may be seen in up to 15-37% of systolic heart failure patients (2,3). A longer cycle length, usually between 45-90 seconds, as well as the waxing and waning breathing pattern differentiate CSR from other forms of cyclic central apnea. CSA leads to chronically increased sympathetic activity and exerts multiple deleterious effects on the failing heart (2). The presence of CSR has been associated with higher mortality and rapid deterioration in cardiac function (4).

Jared Bartell and Safal Shetty, MD

University of Arizona Medical Center

Tucson, AZ

References

1. Berry RB, Budhiraja R, Gottlieb DJ, Gozal D, Iber C, Kapur VK, Marcus CL, Mehra R, Parthasarathy S, Quan SF, Redline S, Strohl KP, Davidson Ward SL, Tangredi MM; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597-619. [CrossRef]  [PubMed]
2. Yumino D, Bradley TD. Central sleep apnea and Cheyne-Stokes respiration. Proc Am Thorac Soc. 2008;5(2):226-36. [CrossRef] [PubMed]
3. Garcia-Touchard A, Somers VK, Olson LJ, Caples SM. Central sleep apnea: implications for congestive heart failure. Chest. 2008;133(6):1495-504. [CrossRef] [PubMed]
4. Hanly PJ, Zuberi-Khokhar NS. Increased mortality associated with Cheyne-Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med. 1996;153(1):272-6. [CrossRef] [PubMed] 

Reference as: Bartell J, Shetty S. Medical image of the week: Cheyne-Stokes respiration. Southwest J Pulm Crit Care. 2015;10(3):145-6. doi: http://dx.doi.org/10.13175/swjpcc017-15 PDF

Medical Image of the Week: Metastatic Collecting Duct Carcinoma

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Figure 1. Transverse section of CT chest and abdomen shows enhancing pleural nodularity (yellow arrows) with a pleural effusion.

Figure 2.  Transverse section of CT abdomen shows heterogeneous enhancing mass in the right kidney (red arrow).

Figure 3. Coronal section of CT chest and abdomen showing a large right pleural effusion (yellow arrow) and atelectatic lung with mediastinal shift to the left. Red arrow points to the heterogeneous mass in the right kidney.

A 40-year-old woman home health nurse presented to the ED with intermittent right sided sharp chest pain and progressive dyspnea for 2 weeks. On admission she was found to be in respiratory distress. Chest x-ray revealed a massive right sided pleural effusion. Thoracic CT scan with contrast confirmed a large right pleural effusion with associated enhancing pleural nodularity also involving the diaphragmatic surface (Figure 1).  The visualized part of the abdomen revealed a mass in the midpole of right kidney (Figure 2). Subsequent CT scan of the abdomen with contrast revealed a heterogeneous enhancing mass in the right kidney suspicious for malignancy (Figure 3) and multiple paracaval lymph nodes. Thoracentesis revealed a hemorrhagic pleural effusion and during subsequent right video-assisted thoracoscopy showed disseminated tumorlets along the diaphragm and pleura. Pleural biopsy and fluid cytology was consistent with metastatic poorly differentiated collecting duct carcinoma of the kidney. The patient is currently getting outpatient chemotherapy. Collecting duct carcinoma of the kidney is an unusual variant of renal cell carcinoma and accounts for about 1% of all renal cell carcinomas (1). This variant has a poor prognosis and frequently metastasizes to the lung and liver.

Chandramohan Meenakshisundaram, MD

Nanditha Malakkla, MD

St. Francis Hospital.

Evanston, IL

Reference

1. Wang X, Hao J, Zhou R, Zhang X, Yan T, Ding D, Shan L, Liu Z. Collecting duct carcinoma of the kidney: a clinicopathological study of five cases. Diagn Pathol. 2013;8:96. [CrossRef] [PubMed]

Reference as: Meenakshisundaram C, Malakkla N. Medical image of the week: metastatic collecting duct carcinoma. Southwest J Pulm Crit Care. 2014;9(6):348-9. doi: http://dx.doi.org/10.13175/swjpcc160-14 PDF