Medical Image of the Week: Cannon V Waves

Figure 1. Video showing jugular venous distention to earlobes with cannon V waves.

A 66-year-old man experienced recurrent ascites of unknown etiology over six months. He had previously undergone a renal transplant secondary to complications of diabetes and hypertension and had known severe coronary artery disease. His most recent paracentesis revealed an albumin 1.6 g/dL (serum albumin 2.1) and a total protein of 3.8 g/dL. His adenosine deaminase was 11.6 U/L (normal <7.6 U/L), but repeated bacterial and mycobacterial ascites cultures were negative, as were a carcinoembryonic antigen assay and ascites cytology. Computerized tomography of the abdomen showed findings consistent with cirrhosis, but an extensive workup for common causes of cirrhosis was negative.

Physical exam showed jugular venous distention with prominent V waves and a holosystolic murmur at the left lower sternal border (Figure 1). Echocardiography showed a dilated right ventricle, moderate pulmonary and tricuspid regurgitation and an estimated right ventricular systolic pressure of 87 mm Hg. Cardiac catherization confirmed the presence of an elevated right ventricular pressure of 72/10 (22) mm Hg, an elevated pulmonary artery pressure of 75/27 (45) mm Hg and a left ventricular ejection fraction of 20-25%. The right atrial pressure was 20 and the pulmonary artery occlusion pressure was 22 mmHg.  A diagnosis of pulmonary hypertension secondary to left ventricular heart disease (type 2 pulmonary hypertension) with congestive hepatopathy and cardiac ascites was made.

The patient’s physical examination provided an important clue to the etiology of the ascites – cardiac ascites is thought to be due to chronic venous congestion of the liver due to transmission of high central venous pressures. Tricuspid regurgitation can be associated with severe hepatic congestion because of retrograde transmission of right ventricular pressure directly into the hepatic veins. In some patients (although not in this patient), careful examination will reveal that the liver in such patients is palpably pulsatile.

Cardiac ascites is typically characterized by a serum albumin gradient (SAAG) >1.1 g/dL (indicative of portal hypertension) and ascites protein level of >2.5 g/dL (1). We cannot fully explain why this patient’s SAAG was low. A complete workup for infectious and oncological etiologies of low SAAG ascites was negative. It has been noted that in patients with known cirrhosis (as in this patient), the finding of a low SAAG has a low specificity for infectious and oncological etiologies of ascites (2). Serositis which can sometimes manifest as ascites can also be a complication of tacrolimus which the patient was receiving s/p renal transplant. It’s possible that tacrolimus might have changed the nature of the ascites fluid in this patient but this is conjectural. 

Robert A. Raschke, MD

College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Sam AH, James THT. Rapid Medicine. Wiley-Blackwell; 2009: ISBN 1-4051-8323-3.
2. Khandwalla HE, Fasakin Y, El-Serag HB. The utility of evaluating low serum albumin gradient ascites in patients with cirrhosis. Am J Gastroenterol. 2009 Jun;104(6):1401-5. [CrossRef] [PubMed] 

Cite as: Raschke RA. Medical image of the week: cannon V waves. Southwest J Pulm Crit Care. 2017;15(2):90-1. doi: https://doi.org/10.13175/swjpcc095-17 PDF

Medical Image of the Week: Hepatic Hydrothorax

Figure 1. Panel A: Chest x-ray showing right pleural effusion. Panel B: Coronal view of the thoracic CT scan in soft tissue windows showing right pleural effusion.

Figure 2. Nuclear scan after intraperitoneal injection of technetium 99mTc albumin aggregated (99mTc-MAA). After less than one hour most of the tracer migrated into the right hemithorax consistent with hepatic hydrothorax.

A 63 year-old woman, with known alcoholic liver cirrhosis, esophageal varices with history of banding presented to an outside hospital with progressive shortness of breath, and was found to have a large right transudative pleural effusion. The patient underwent 2 diagnostic and therapeutic thoracenteses within 3 days, removing 1100 ml and 1500 ml respectively. No ascites was present. At the time of admission the patient had recurrent right effusion (Figure 1). Abdominal ultrasound showed minimal free intrabdominal fluid and she had signs of third spacing on her lower extremities. The patient underwent intraperitoneal injection of Technetium 99mTc albumin aggregated (99mTc-MAA). After less than one hour most of the tracer migrated into the right hemithorax consistent with hepatic hydrothorax (Figure 2).

While the exact mechanism involved in the development of hepatic hydrothorax is incompletely understood, it probably results from the passage of ascitic fluid from the peritoneal into the pleural cavity through small diaphragmatic defects. These are typically < 1 cm (and may be microscopic) and are generally located in the tendinous portion of the diaphragm. The negative intrathoracic pressure generated during inspiration favors the passage of the fluid into the pleural space. Thus, patients may have only mild or clinically undetectable ascites.

Once the diagnosis is made treatment follows algorithms for treatment of refractory ascites and include salt and water restriction, diuretics, and other validated options for portal hypertension. Repeated thoracentesis and chest tube placement is discouraged.

Huthayfa Ateeli, Justin Lee, Irbaz Riaz, Meenal Misal

Department of Internal Medicine

University of Arizona

Tucson, AZ

References

1. Huang PM, Chang YL,Yang CY,Lee YC.The morphology of diaphragmatic defects in hepatic hydrothorax: thoracoscopic finding. J Thorac Cardiovasc Surg. 2005;130:141-5. [CrossRef] [PubMed]
2. Lieberman FL, Hidemura R, Peters RL, Reynolds TB. Pathogenesis and treatment of hydrothorax complicating cirrhosis with ascites. Ann Intern Med. 1966;64:341-51. [CrossRef] [PubMed]
3. Emerson PA, Davies JH. Hydrothorax complicating ascites. Lancet. 1955; 268:487-8. [CrossRef] [PubMed]
4. Mouroux J, Perrin C, Venissac N, Blaive B, Richelme H. Management of pleural effusion of cirrhotic origin. Chest. 1996;109:1093-6. [CrossRef] [PubMed]
5. Chen A, Ho YS, Tu YC, Tang HS, Cheng TC. Diaphragmatic defect as a cause of massive hydrothorax in cirrhosis of liver. J Clin Gastroenterol. 1988;10:663-6. [CrossRef] [PubMed] 

Reference as: Ateeli H, Lee J, Riaz I, Misal M. Medical image of the week: hepatic hydrothorax. Southwest J Pulm Crit Care. 2015;10(1):47-8. doi: http://dx.doi.org/10.13175/swjpcc004-15 PDF