Medical Image of the Week: Extrapleural Pneumolysis for Tuberculosis

Figure 1. PA (A)/Lateral (B) chest films showing a mass like opacity of the left upper lung field.

Figure 2. Representative image from the thoracic CT in soft tissue windows showing a well-circumscribed, oval-shaped, heterogeneous density within the left upper and mid anterior chest with some expansion and destruction of overlying ribs.

The advent of antibiotics revolutionized the management of tuberculosis, a disease that even in the 1950s was a top 10 cause of death in the United States. The first drug to be developed was streptomycin, approved after a clinical trial in 1946. The following decade saw the addition of ethambutol, rifampin, and isoniazid (1). Though we take for granted the use our multidrug regimens nowadays, physicians once had limited interventions for this frequent and devastating infection. Such interventions included surgical techniques to collapse the affected lobes, starving the mycobacterium of their preferred oxygen rich environment. One such technique was known as plombage, or extrapleural pneumolysis. Plombage is a term derived from the Latin for lead or plumbum and entails the insertion of a space occupying material into the pleural space with subsequent compression of the affected lung portion. This was seen as an alternative to the use of thoracoplasty, which required removal of multiple ribs allowing the chest wall to collapse, leading to deformity and a loss of lung function (2). Though rarely seen now, we present the imaging of an elderly female with endometrial cancer with lung metastasis who interestingly had undergone such a procedure when she developed cavitary tuberculosis as a teenager in 1952.

Tuffler first developed extrapleural pneumolysis in 1891; he placed fat into the pleural cavity reporting successful control of tuberculosis infection. The technique over the subsequent decades became popular especially as a response to the endemic tuberculosis seen post- the Second World War. Many attempts were made to designate an ideal inert material for use. Though unclear in our patient given the remote history of the procedure, published reports include placement of muscle, fat, air, mineral oil, gauze, paraffin, rubber sheeting, and even inflated Lucite balls. Fortunately, complications of the procedure, even decades later, are rarely seen now. Complications listed in the literature, however, do include infection, hemorrhage, fistula formation, migration of material, and even malignancy. Despite its popularity, there were mixed results in effectiveness and variable complication rates, in one series nearly 50% of patients developed an infection (3). In our patient, it was successful, with no history of recurrence with negative sputum and serologic testing. She did notably report having been treated with a long course of antibiotics as well.

Kareem Ahmad, MD

Department of Internal Medicine

Division of Pulmonary, Critical Care, Sleep, and Allergy Medicine

University of Arizona

Tucson, AZ, USA

References

1. Zumla A, Nahid P, Cole ST. Advances in the development of new tuberculosis drugs and treatment regimens. Nat Rev Drug Discov. 2013 May;12(5):388-404. [CrossRef] [PubMed]
2. Young FH. Extraperiosteal plombage in the treatment of pulmonary tuberculosis. Thorax. 1958; 13(2):130-5. [CrossRef] [PubMed]
3. Murphy JD, Elrod PD, et al. Surgical treatment of residual cavities following thoracoplasties for tuberculosis. Dis Chest. 1948 Sep-Oct;14(5):694-706. [CrossRef] [PubMed]

Cite as: Ahmad K. Medical image of the week: extraplerural pneumolysis for tuberculosis. Southwest J Pulm Crit Care. 2016;13(5):244-5. doi: https://doi.org/10.13175/swjpcc106-16 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