3-year-old Domestic Longhair cat
Presented for ptyalism, possible lily intoxication. Two days later tachypneic with fever.
The cat initially presented to the emergency service for ptyalism and possibly lily ingestion. Activated charcoal was administered via nasoesophageal tube, after the cat was sedated. Bloodwork showed mild azotemia but urine specific gravity was normal (pre-renal azotemia). The cat was hospitalized for intravenous fluid therapy. Two days later, the cat became tachypneic, lethargic and developed a fever. Thoracic radiographs revealed asymmetric bilateral pleural effusion, worse on the right, in addition to cranioventral lung consolidation, which was also worse on the right. Due to concern over possible esophageal perforation during passing of the nasoesophageal tube, esophagraphy with non-ionic iodinated contrast medium was performed; no areas of perforation were identified. Cytology on the pleural effusion showed septic exudate with abundant extracellular material most consistent with charcoal. Bilateral chest tubes were placed and the patient was treated with antibiotics and other supportive therapies. Endotracheal wash two days later showed chronic neutrophilic inflammation and extracellular material consistent with charcoal. Due to lack of response to medical therapy and declining clinical status (sepsis/SIRS), CT followed by exploratory thoracotomy was performed.
CT protocol: Transverse images of the thorax were acquired with 2.5mm detail algorithm, 1.25mm high resolution algorithms pre and post intravenous contrast. CT esophagography was performed with non-ionic iodinated contrast medium and additional series were obtained.
Chest tubes are present bilaterally. There is moderate bilateral pleural effusion. A small amount of free gas is present in the pleural space (+ / – caudal mediastinum), particularly in the right caudomedial thorax in the region of the accessory lung lobe. On pre-contrast images, there is wispy hyperattenuating (HU ~80) material in the ventral thorax, more extensive caudal to the heart. This material is at least partly due to thickening of the ventral mediastinal tissues, based on the presence of contrast enhancement in some areas (post HU ~130); some of the material is also suspected to be within the pleural space. There are areas of mild costal pleural thickening (for example, see pre contrast series, along the right and left ventrolateral aspects), which are mildly hyperattenuating relative to the pleural fluid on pre contrast images and are mildly contrast enhancing.
The lung lobes are partially collapsed, with either areas of alveolar pattern (seen especially in the more ventral lung field, right worse than left). The visceral margins of the lung lobes are generally irregular and/or rounded. There is also thickening of the pulmonary pleura (for example, see post contrast series, along the medial aspect of the right caudal lung lobe). In the right caudodorsal thorax, ventrolateral to the esophagus, there is a triangular hyperattenuating structure (HU ~120-170) with small internal gas bubbles (a vesicular-like pattern) that likely is an abnormal portion of the accessory lung lobe; this area does not enhance post-contrast. The branch of the accessory lobe bronchus coursing to this portion of the lobe is visible more cranially, but then is not seen just cranial to or within this abnormal portion of the lung lobe. The rest of the accessory lobe is consolidated, similar to the other lobes, and the bronchus to this portion of the lobe is more clearly seen.
The sternal and cranial mediastinal lymph nodes are mild to moderately enlarged and heterogeneously contrast enhancing.
On the esophagram series, there is no leakage of contrast seen. A gastrotomy tube is in place.
- Bilateral pleural effusion, consistent with the reported septic effusion. The hyperattenuating material in the ventral thorax and along the pleura may be charcoal. Secondary pleuritis (pulmonary, costal, mediastinal) is present.
- The hyperattenuating, non-contrast enhancing portion of the accessory lung lobe with a vesicular-like gas pattern is suspect for charcoal deposition with necrosis and/or secondary infection. Lack of visualization of part of the bronchus to this portion of the lung lobe may be secondary to luminal fluid or debris and/or bronchial collapse.
- Multilobar lung consolidation is likely in part due to collapse secondary to the effusion. The irregular and/or rounded contour of the lung margins may be due to a restrictive/fibrosing pleuritis and this could be contributing to lobar consolidation. Secondary bronchopneumonia is another possibility.
- Small pneumothorax +/- pneumomediastinum, which may be partly iatrogenic due to the presence of chest tubes. It may also be due to leakage from the abnormal portion of the accessory lung lobe. Pneumothorax is not due to esophageal perforation, since perforation was not documented on this study nor on the prior radiographic study.
- Sternal and cranial mediastinal lymph nodes are likely reactive
CT images of a syringe of activated charcoal were obtained after patient imaging, in order to ascertain its Hounsfield units (HU ~ 105-110). The high HU helped in confirming the theory that inadvertent deposition of activated charcoal into the dorsal portion of the accessory lung lobe had occurred during supposed nasoesophageal intubation. This presumably led to lung lobe necrosis and subsequent leakage of charcoal into the pleural space, initiating a severe, septic pleuritis. Lack of coughing during the inadvertent tracheal intubation may have been due to the fact that the cat was sedated during the procedure.
After CT, the patient was taken for exploratory thoracotomy. Black fibrinous-like material consistent with charcoal was found throughout the entire thoracic cavity, along all pleural surfaces, and severe pleuritis was present. The caudodorsal portion of the accessory lung lobe appeared necrotic and black in color. The lung lobe was friable and after lobectomy, black material (charcoal) was readily oozing from the lung tissue. Other lung lobe surfaces were friable secondary to the pleuritis and during debridement of the right caudal lung lobe, tearing of the lung occurred, so this lung also had to be removed. Debridement of the various pleural surfaces was performed, along with flushing of the pleural space.
Histopathology of the accessory lobe showed severe, chronic active, necrotizing and interstitial pneumonitis with intralesional black material (charcoal). The right caudal lung lobe showed severe subacute pleuritis and aggregates of charcoal were seen in the pleura. The cat improved post-operatively and was eventually sent home.
The cat was re-examined on multiple occasions within a year post surgery and was doing well at home. A chronic intermittent cough was present, but this was reportedly present prior to surgery (patient had presumptive lower airway disease prior to this incident). Serial follow-up radiographs showed gradual re-expansion of the lung as well as compensatory hyperinflation of the right middle and cranial lobes; only minimal residual pleural opacity and pleural fissure lines were seen.
Inadvertent tracheal intubation is a known potential complication of esophageal tube placement and radiographs are generally recommended to check tube location prior to instillation of any substances. Coughing would be expected with tracheal intubation and could alert a clinician to possible misplacement of a tube, but may not have occurred in this cat because he was sedated. Although instillation of activated charcoal into the lungs has not been reported in animals, it has been reported in human patients. Most of the case reports regarding this condition describe the long term complications, which include chronic inflammatory lung disease and bronchiolitis obliterans organizing pneumonia (now known as cryptogenic organizing pneumonia). Activated charcoal has even been used in rodent research and can serve as a model for BOOP. One brief description was found regarding the lung appearance in acute charcoal aspiration and on CT, there was pleural effusion and dense consolidation in one lung lobe, with an HU of ~130, similar to the appearance in this case.
Severe pleuritis is more common in dogs and cats with pyothorax (such as secondary to direct inoculation from penetrating injury or bite wound, pneumonia, migrating foreign body, ruptured esophagus) or chylothorax, among other causes. There is one case report of a dog with pleuritis associated with birefringent material, which had histologic findings similar to cases of asbestosis in humans. Restrictive/fibrosing pleuritis can occur secondary to severe pleural inflammation and has been described mostly in cases with chylothorax. Lung lobes can have varying degrees of collapse, rounded or irregular margins, pleural thickening or persistent lobar collapse despite removal of pleural effusion. In this cat, the lungs did gradually re-inflate over the 12 months post surgery, so the presence of a real or permanent restrictive pleuritis did not appear to be present. This was likely at least in part due to surgical debridement of the black fibrinous-like material from the various pleural surfaces at surgery.
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