Medical Image of the Week: Actinomycosis

Figure 1. Thoracic CT scan showing right-sided necrotizing pneumonia, lung abscess and empyema (arrows).

Figure 2. Cytospin and cell block of right lower lobe bronchoalveolar lavage fluid stained with Grocott-Gomori's (or Gömöri) methenamine silver (GMS) stain showing positive filamentous organisms consistent with Actinomyces species within a background of inflammatory cells.

Figure 3. Low (Panel A) and high power view (Panel B) of the lung showing alveolar septa filled with predominantly acute (neutrophilic) infiltrate.

A 55-year-old man with history of tobacco and alcohol abuse, presented with unresolving pneumonia despite treatment with moxifloxacin. It was thought to be possible coccidioidomycosis and an azole was started. However, he returned with increasing dyspnea and hypoxemia. He had leukocytosis with a thoracic CT revealing a loculated empyema, multifocal necrotizing infection and a large intrapulmonary abscess (Figure 1). He was admitted to MICU, intubated and ventilated. He was in septic shock requiring fluid resuscitation, vasopressors, and broad antibiotics. Bronchoscopy revealed erythematous and edematous airways, with drainage of over one liter of purulent fluid. A chest tube was placed to drain pleural fluid with removal of around two liters of blood-tinged, purulent fluid. His condition worsened with development of disseminated intravascular coagulation leading to hemorrhagic shock. He arrested and died. Gram stain on bronchoalveolar lavage fluid showed mixed gram negative and gram variable rods, and cultures grew lactobacillus species. GMS stain revealed filamentous organisms consistent with Actinomyces (Figure 2).

Necrotizing pneumonia is usually secondary to aspiration of oral bacterial flora, and is usually associated with severe sepsis and acute respiratory failure. The obstruction of the bronchus and blood vessels corresponding to a lung segment leads to decreased perfusion that is often shown on contrast enhanced CT scan. Hence, systemic antibiotic treatment alone is usually not effective. The management of necrotizing pneumonia is multidisciplinary; including adequate antibiotic therapy, mechanical ventilation, closed pleural drainage and supportive care. Despite the serious morbidity, massive parenchymal damage and prolonged hospitalizations, long-term outcome following necrotizing pneumonia is good with multidisciplinary care. If initial medical therapy fails, surgery is a reasonable option. Resection of gangrenous lung parenchyma and drainage of pleural empyema can lead to recovery in up to 80% of patients. Rarely, lobectomy can be a salvage operation. Outcome is affected by the severity of disease and underlying comorbidities. It should be considered once operative risk is acceptable.

Tauseef Afaq Siddiqi MD^1,2, Tracy Lundberg MD³, Jennifer Thorn MD³, and Dena L’heureux MD^1,2

¹Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, The University of Arizona Medical Center, Tucson, AZ

²Department of Medicine, Southern Arizona Veterans Administration Health Sciences Center, Tucson, AZ

³Department of Pathology, The University of Arizona Medical Center, Tucson, AZ

References

1. Alifano M, Lorut C, Lefebvre A, Khattar L, Damotte D, Huchon G, Regnard JF, Rabbat A. Necrotizing pneumonia in adults: multidisciplinary management. Intensive Care Med. 2011;37(11):1888-9. [CrossRef] [PubMed]
2. Schweigert M, Dubecz A, Beron M, Ofner D, Stein HJ. Surgical Therapy for Necrotizing Pneumonia and Lung Gangrene. Thorac Cardiovasc Surg. 2013;61(7):636-41. [CrossRef] [PubMed]
3. Tsai YF, Ku YH. Necrotizing pneumonia: a rare complication of pneumonia requiring special consideration. Curr Opin Pulm Med. 2012;18(3):246-52. [CrossRef] [PubMed]

Reference as: Siddiqi TA, Lundberg T, Thorn J, L’heureux D. Medical image of the week: actinomycosis. Southwest J Pulm Crit Care. 2015;10(5):302-3. doi: http://dx.doi.org/10.13175/swjpcc050-15 PDF

Medical Image of the Week: Tumor-Induced Hypoglycemia

 

Figure 1. CT of the abdomen with IV contrast (axial image) demonstrating numerous large enhancing liver metastases (red oval) and tumor thrombus in the anterior segment branch of the right portal vein (arrow).

A 39 year-old man with a history of widely metastatic (brain, liver and lung) nonseminomatous germ cell tumor was admitted to the hospital with severe abdominal pain and altered mental status. A CT of the abdomen and pelvis with IV contrast revealed a marked increase in the size of the liver metastases, portal vein tumor thrombus and changes of pseudocirrhosis. There were numerous large heterogeneously enhancing masses within the liver parenchyma with central necrosis (Figure 1).

The patient had significant and sustained hypoglycemia, with the lowest glucose recorded of 30 mg/dl. He required multiple IV doses of 50% dextrose and an infusion of 10% dextrose to maintain a serum glucose level greater than 55 mg/dl. His mental status improved with treatment of the hypoglycemia. The patient decided to pursue a palliative approach to care and was discharged with home hospice services.

Tumor-induced hypoglycemia (TIH) is a paraneoplastic syndrome that is uncommon in clinical practice (1). The more common cause of TIH is insulin hypersecretion in the setting of pancreatic beta-cell tumors. Mechanisms that may lead to TIH without insulin hypersecretion include the hypersecretion by tumors of insulin-like growth factor 2 (IGF2) and it’s precursors, insulin-like growth factor 1 (IGF1), somatostatin, and glucagon-like peptide 1. Other pathogenic causes of hypoglycemia include tumor autoimmune hypoglycemia, massive tumor burden, massive tumor liver infiltration, and pituitary or adrenal gland destruction by the tumor. TIH unrelated to pancreatic tumors is called non-islet-cell tumor hypoglycemia (NICTH). The most common cause of NICTH is the hypersecretion of IGF2 and IGF2 precursors by the tumor. This results in increased glucose consumption peripherally and decreased production of glucose in the liver. We did not measure levels of IGF2 in our patient. It was felt the most likely cause of his hypoglycemia was extensive tumor invasion and destruction of the liver due to his advanced disease.

Pavan Parashar MD¹, Meghan Bullock BSN, RN, OCN, Linda Snyder MD²

¹Department of Medicine, Geriatrics, Palliative and General Medicine, Banner University Medical Center-Tucson

²Department of Medicine, Pulmonary, Critical Care and Palliative Medicine, Banner University Medical Center-Tucson

Reference

1. Iglesias P, Díez JJ. Management of endocrine disease: a clinical update on tumor-induced hypoglycemia. Eur J Endocrinol. 2014;170(4):R147-57. [CrossRef] [PubMed] 

Reference as: Parashar P, Bullock M, Snyder L. Medical image of the week: tumor-induced hypoglycemia. Southwest J Pulm Crit Care. 2015;10(5):300-1. doi: http://dx.doi.org/10.13175/swjpcc049-15 PDF