Lung Lobe Torsion

Lung lobe torsion (LLT) is a rare but life-threatening condition characterized by rotation of a pulmonary lobe around its bronchovascular pedicle, resulting in obstruction of the bronchus, pulmonary artery, and pulmonary vein. This rotation leads to venous congestion, ischemia, and ultimately necrosis of the affected lobe. The condition is most commonly seen in dogs, with a predilection for large, deep-chested breeds, and is rarely reported in cats. LLT can occur as a primary (idiopathic) event or secondary to underlying thoracic pathology such as pleural effusion, trauma, or previous thoracic surgery. The right middle lung lobe is most frequently affected, followed by the left cranial lobe. The rotation typically occurs around the long axis of the lobe, but can also involve the hilus. The resultant vascular compromise leads to a cascade of events including pulmonary hemorrhage, edema, and infarction, which can rapidly progress to systemic inflammatory response syndrome (SIRS) and death if not treated promptly. Surgical intervention, typically lobectomy, is the definitive treatment and carries a favorable prognosis if performed before irreversible necrosis and systemic complications ensue.

The exact etiology of lung lobe torsion is often multifactorial. Primary (idiopathic) torsion occurs without identifiable underlying cause, but is hypothesized to result from congenital or acquired laxity of the pulmonary ligament, which normally anchors the lung lobes to the mediastinum. Secondary torsion is associated with conditions that alter the normal thoracic anatomy or physiology, including: (1) pleural effusion (e.g., chylothorax, pyothorax, hemothorax) which can cause atelectasis and increase mobility of the lung lobes; (2) thoracic trauma leading to diaphragmatic hernia or pulmonary contusions; (3) previous thoracic surgery, particularly thoracotomy or median sternotomy, which may disrupt normal adhesions; (4) pulmonary masses or bullae that alter lobar weight and position; (5) chronic respiratory disease such as bronchitis or asthma causing air trapping and hyperinflation; (6) iatrogenic causes, such as over-inflation of the lung during anesthesia or mechanical ventilation. The biomechanical trigger for torsion is likely a combination of increased mobility of the lobe and a sudden change in intrathoracic pressure or body position, which initiates the rotational force. Once the lobe rotates, venous outflow obstruction leads to progressive congestion and edema, further increasing lobar weight and perpetuating the torsion.

Lung lobe torsion is an uncommon condition in small animal practice, with a reported incidence of less than 0.1% in dogs. It is most frequently diagnosed in large and giant breed dogs, particularly those with deep chests such as Afghan Hounds, Borzois, Great Danes, and Irish Wolfhounds. However, it can occur in any breed, including small breeds and cats, albeit rarely. There is no clear sex predilection, but some studies suggest a slight male predominance. The age at presentation is variable, ranging from young adults to geriatric patients, with a median age of 5-7 years. In cats, the condition is extremely rare, with only isolated case reports. The right middle lung lobe is the most commonly affected (approximately 50% of cases), followed by the left cranial lobe (approximately 25%), and less commonly the right cranial or caudal lobes. Bilateral or multiple lobe torsions are exceedingly rare. The condition is often associated with concurrent thoracic pathology, such as chylothorax or pyothorax, which may predispose to torsion. In a retrospective study of 32 dogs with lung lobe torsion, 53% had concurrent pleural effusion, and 22% had a history of prior thoracic surgery. The mortality rate in untreated cases approaches 100%, but with prompt surgical intervention, the prognosis is good, with a reported survival rate of 80-90%.

The pathophysiology of lung lobe torsion involves a complex interplay of vascular, bronchial, and parenchymal changes. The initial event is rotation of the lobe around its pedicle, which contains the bronchus, pulmonary artery, and pulmonary vein. The rotation, typically 180 to 360 degrees, causes partial or complete obstruction of these structures. The pulmonary artery, being a high-pressure system, may remain partially patent initially, allowing continued arterial inflow, while the low-pressure pulmonary vein is more easily compressed, leading to venous outflow obstruction. This results in severe venous congestion, increased capillary hydrostatic pressure, and transudation of fluid into the interstitium and alveoli, causing pulmonary edema and hemorrhage. The bronchus becomes obstructed, leading to air trapping and atelectasis distal to the obstruction. The combination of ischemia, venous congestion, and air trapping leads to rapid parenchymal necrosis. Histologically, the affected lobe shows diffuse alveolar hemorrhage, edema, and necrosis of alveolar walls, with thrombosis of pulmonary vessels. The necrotic lobe becomes a nidus for bacterial translocation and release of inflammatory mediators, which can trigger systemic inflammatory response syndrome (SIRS), sepsis, and disseminated intravascular coagulation (DIC). If the torsion is not relieved, the condition is rapidly fatal. Surgical removal of the affected lobe is essential to halt the progression of systemic inflammation and restore normal pulmonary function.

Several factors may predispose an animal to lung lobe torsion. Intrinsic factors include: (1) conformational characteristics, such as a deep, narrow chest, which may allow greater mobility of the lung lobes; (2) congenital or acquired laxity of the pulmonary ligament, which normally anchors the caudal lobes to the mediastinum; (3) chronic respiratory disease, such as bronchitis or asthma, leading to air trapping and hyperinflation of lobes; (4) obesity, which may increase intra-abdominal pressure and alter thoracic dynamics; (5) age-related degenerative changes in the pulmonary parenchyma. Extrinsic factors include: (1) thoracic trauma, such as blunt force injury or diaphragmatic hernia, which can disrupt normal thoracic anatomy; (2) pleural effusion of any cause (chylothorax, pyothorax, hemothorax), which can cause atelectasis and increase lobar mobility; (3) previous thoracic surgery, particularly thoracotomy or median sternotomy, which may disrupt normal adhesions and create a mobile lobe; (4) iatrogenic factors, such as over-inflation of the lung during anesthesia or mechanical ventilation; (5) the presence of pulmonary masses or bullae, which can alter lobar weight and position. In many cases, no obvious predisposing factor is identified, and the torsion is considered idiopathic.

The clinical signs of lung lobe torsion are often acute and severe, but can be insidious in some cases. Common presenting signs include: (1) acute onset of respiratory distress, characterized by tachypnea, dyspnea, and open-mouth breathing; (2) coughing, which may be productive or non-productive; (3) hemoptysis, which is reported in up to 30% of cases; (4) lethargy and depression; (5) anorexia; (6) fever, which may be due to necrosis and inflammation; (7) cyanosis in severe cases. On physical examination, findings may include: (1) increased respiratory effort with abdominal component; (2) auscultation reveals muffled lung sounds over the affected lobe, and possibly crackles or wheezes due to pulmonary edema; (3) dullness on thoracic percussion over the affected area, suggesting consolidation or effusion; (4) tachycardia and weak pulses due to hypovolemia or sepsis; (5) signs of systemic inflammatory response syndrome (SIRS), such as elevated heart rate, respiratory rate, and temperature, or hypothermia. In chronic cases, weight loss and intermittent coughing may be observed. The severity of clinical signs depends on the degree of torsion, the lobe affected, and the presence of concurrent thoracic pathology. In some cases, the condition may be an incidental finding on thoracic imaging performed for other reasons.

The differential diagnoses for lung lobe torsion include: (1) Pulmonary thromboembolism (PTE): Presents with acute respiratory distress and may have risk factors such as hyperadrenocorticism, heart disease, or sepsis. Imaging may show oligemia in affected lung regions, but no lobar consolidation or torsion. CT angiography is diagnostic. (2) Severe pneumonia or lung abscess: May cause lobar consolidation on radiographs, but clinical signs are usually more chronic and include fever, productive cough, and leukocytosis. Bronchoscopy and BAL may reveal infectious agents. (3) Pulmonary neoplasia: Primary or metastatic lung tumors can cause lobar consolidation or mass effect. CT and biopsy are necessary for diagnosis. (4) Atelectasis due to pleural effusion or pneumothorax: Radiographs show lobar collapse, but the lobe is not rotated. Thoracocentesis and imaging can differentiate. (5) Diaphragmatic hernia: May cause displacement of lung lobes and respiratory distress. Radiographs may show loss of diaphragmatic outline and herniated abdominal organs. (6) Chylothorax or pyothorax: Can cause pleural effusion and secondary atelectasis, but the underlying cause must be identified. Thoracocentesis and analysis of fluid are essential. (7) Foreign body aspiration: May cause lobar collapse or consolidation. Bronchoscopy can identify and remove the foreign body. (8) Lung lobe torsion must be differentiated from these conditions by imaging, particularly CT, which can show the characteristic twisted bronchovascular pattern and lobar consolidation.

The diagnostic algorithm for lung lobe torsion begins with a thorough history and physical examination, with emphasis on respiratory and cardiovascular systems. If LLT is suspected, the following steps are recommended: (1) Thoracic radiographs (three views: right lateral, left lateral, and ventrodorsal or dorsoventral) are the initial imaging modality. Classic radiographic findings include lobar consolidation, air bronchograms, and a characteristic 'twisted' or 'kinked' bronchus. The affected lobe may appear as a soft tissue opacity with a lobar border, and there may be evidence of pleural effusion. However, radiographs are not always diagnostic, and false negatives can occur. (2) If radiographs are inconclusive or if the patient is stable, computed tomography (CT) of the thorax is the gold standard for diagnosis. CT findings include a twisted bronchovascular pattern, lobar consolidation, and a 'beak' sign at the hilus. CT also allows for evaluation of concurrent thoracic pathology. (3) Thoracic ultrasound may be useful in identifying lobar consolidation and pleural effusion, but is not definitive for torsion. (4) Bronchoscopy can be performed to visualize the twisted bronchus, but is not always necessary and may be contraindicated in unstable patients. (5) Laboratory tests, including CBC, serum biochemistry, and coagulation profile, are performed to assess systemic health and identify complications such as SIRS or DIC. (6) If the patient is unstable, emergency surgery may be indicated based on clinical signs and imaging findings, without further diagnostic testing. The definitive diagnosis is confirmed at surgery by visualization of the twisted lobe.

Laboratory findings in lung lobe torsion are non-specific but may reflect the severity of the condition. Complete blood count (CBC) may reveal leukocytosis with a left shift, or leukopenia in severe cases, indicating systemic inflammation or sepsis. Anemia may be present due to hemorrhage into the lung lobe. Serum biochemistry may show elevated liver enzymes (ALT, AST) due to hypoxia or SIRS, and elevated creatinine and BUN if there is prerenal azotemia from dehydration or shock. Electrolyte imbalances, such as hyponatremia or hyperkalemia, may occur due to vomiting or renal dysfunction. Coagulation profile (PT, aPTT, platelet count, and D-dimer) may be abnormal, with prolonged PT/aPTT and thrombocytopenia indicating DIC. Blood gas analysis may reveal hypoxemia and hypercapnia due to impaired gas exchange. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated. Thoracocentesis, if pleural effusion is present, yields a modified transudate or exudate, which may be hemorrhagic. Cytology of the fluid may show non-degenerate neutrophils and macrophages, and culture may be negative unless there is secondary infection. These findings are not specific for LLT but help in assessing the patient's overall condition and guiding treatment.

Imaging plays a crucial role in the diagnosis of lung lobe torsion. Thoracic radiographs are the first-line imaging modality. Classic radiographic findings include: (1) lobar consolidation, which appears as a soft tissue opacity with air bronchograms; (2) a 'twisted' or 'kinked' bronchus, which may be seen as an abrupt cutoff or narrowing of the bronchus; (3) displacement of the affected lobe, often with a lobar border that is not in its normal position; (4) pleural effusion, which may obscure the underlying changes; (5) signs of atelectasis in other lobes. However, radiographs are not always diagnostic, and the sensitivity is reported to be around 70-80%. Computed tomography (CT) is the imaging modality of choice for definitive diagnosis. CT findings include: (1) a twisted bronchovascular pattern, where the bronchus and vessels are seen to rotate; (2) lobar consolidation with a 'beak' sign at the hilus; (3) a 'target' sign on cross-sectional images, where the bronchus is surrounded by vessels; (4) enhancement of the affected lobe on contrast studies, which may be absent if there is complete vascular obstruction. CT also allows for evaluation of the entire thorax, including the mediastinum and pleural space, and can identify concurrent pathology such as masses or effusion. Thoracic ultrasound may show a consolidated lobe with a 'hepatized' appearance, but is not specific. Bronchoscopy can be used to visualize the twisted bronchus, but is not always necessary. In summary, CT is the most accurate imaging modality for diagnosing lung lobe torsion and should be performed if the patient is stable enough.

Cytology and histopathology are important for confirming the diagnosis and understanding the pathophysiology of lung lobe torsion. If pleural effusion is present, thoracocentesis and fluid analysis may be performed. The fluid is typically a modified transudate or exudate, with a high protein content and nucleated cell count. Cytology may show non-degenerate neutrophils, macrophages, and red blood cells, consistent with inflammation and hemorrhage. If the fluid is chylous, it will have a high triglyceride content. Histopathology of the affected lung lobe, obtained after surgical resection, reveals characteristic changes: (1) diffuse alveolar hemorrhage and edema; (2) necrosis of alveolar walls and bronchial epithelium; (3) thrombosis of pulmonary vessels; (4) infiltration of neutrophils and macrophages; (5) in chronic cases, fibrosis and organization. These findings are consistent with ischemic necrosis and infarction. In cases of secondary torsion, histopathology may also reveal the underlying cause, such as a pulmonary mass or bulla. Special stains, such as Masson's trichrome, can highlight fibrosis. Histopathology is essential for confirming the diagnosis and ruling out other causes of lobar consolidation, such as neoplasia or pneumonia.

The definitive treatment for lung lobe torsion is surgical resection of the affected lobe (lobectomy). Preoperative stabilization is crucial, especially in patients with respiratory distress or systemic signs. This may include: (1) oxygen supplementation via nasal cannula or oxygen cage; (2) thoracocentesis to remove pleural effusion and improve ventilation; (3) intravenous fluid therapy to correct hypovolemia and electrolyte imbalances; (4) analgesia with opioids (e.g., hydromorphone 0.05-0.1 mg/kg IV q4-6h, or fentanyl CRI 2-5 mcg/kg/h); (5) broad-spectrum antibiotics if there is evidence of infection or necrosis (e.g., ampicillin 22 mg/kg IV q8h, and enrofloxacin 10 mg/kg IV q24h). Surgical approaches include: (1) lateral thoracotomy at the appropriate intercostal space (e.g., 5th or 6th) for access to the right middle or left cranial lobe; (2) median sternotomy for bilateral or multiple lobe involvement. The affected lobe is identified by its dark, congested appearance and twisted pedicle. The pedicle is carefully untwisted to identify the bronchus and vessels. The pulmonary artery and vein are ligated with non-absorbable suture (e.g., 3-0 or 4-0 polypropylene) or vascular clips. The bronchus is then stapled using a thoracoabdominal stapler (TA) or sutured with a simple continuous pattern using 3-0 or 4-0 polydioxanone (PDS). The bronchial stump should be tested for air leaks by filling the thorax with saline and ventilating. A thoracostomy tube is placed for postoperative drainage and monitoring. Postoperative care includes: (1) continued oxygen therapy as needed; (2) pain management with opioids and NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h, or meloxicam 0.1 mg/kg PO q24h); (3) antibiotics for 7-10 days; (4) monitoring for complications such as pneumothorax, hemorrhage, or infection. The prognosis is good if surgery is performed early, with a reported survival rate of 80-90%.

The prognosis for lung lobe torsion is generally good with prompt surgical intervention. In a retrospective study of 32 dogs, the survival rate was 84% for dogs that underwent lobectomy. Factors associated with a poorer prognosis include: (1) delay in diagnosis and treatment; (2) presence of systemic inflammatory response syndrome (SIRS) or disseminated intravascular coagulation (DIC); (3) concurrent thoracic pathology, such as chylothorax or pyothorax; (4) involvement of multiple lobes; (5) postoperative complications, such as bronchial stump leakage or infection. Short-term prognosis is excellent if the patient survives the perioperative period. Long-term prognosis is also good, with most dogs returning to normal activity. However, if the underlying cause (e.g., pleural effusion) is not addressed, there is a risk of recurrence in other lobes. In cats, the prognosis is less well-documented, but is also favorable with surgery. Overall, the prognosis is guarded to good, and early recognition and surgical intervention are key to a successful outcome.

Postoperative follow-up for lung lobe torsion is essential to monitor recovery and detect complications. The thoracostomy tube is typically removed 12-24 hours after surgery, once there is no significant air leak or fluid production. The patient should be monitored closely for respiratory distress, fever, or signs of infection. Serial thoracic radiographs are recommended at 24-48 hours postoperatively to assess lung expansion and check for residual pleural effusion or pneumothorax. Further radiographs may be taken at 2-4 weeks and 8-12 weeks to ensure resolution of any effusion and to evaluate the remaining lung lobes. Activity should be restricted for 2-4 weeks to allow healing of the thoracotomy incision. Pain management should be continued for at least 5-7 days, with a gradual transition from opioids to NSAIDs. Antibiotics are typically continued for 7-10 days. The skin sutures or staples are removed 10-14 days postoperatively. Long-term follow-up is recommended to monitor for recurrence, especially if there is an underlying cause such as chylothorax. In such cases, additional treatment may be necessary, such as thoracic duct ligation or pericardectomy. The owner should be advised to monitor for any signs of respiratory distress, coughing, or lethargy, and to seek veterinary attention if these occur.

Clinical pearls: (1) Always consider lung lobe torsion in any large, deep-chested dog presenting with acute respiratory distress and hemoptysis. (2) Thoracic radiographs may be misleading; if there is a high index of suspicion, proceed to CT or surgery. (3) The right middle lobe is most commonly affected; on radiographs, look for a 'bubble' or 'mass' effect in the cranial mediastinum. (4) At surgery, the affected lobe is dark, congested, and may be twisted; untwist the pedicle to identify the bronchus and vessels. (5) Use a stapler for bronchial closure to reduce the risk of air leak. (6) Place a thoracostomy tube before closing the thorax to manage postoperative pneumothorax or effusion. Pitfalls: (1) Delaying surgery in an unstable patient can lead to irreversible necrosis and systemic complications. (2) Failure to identify and treat concurrent thoracic pathology (e.g., chylothorax) may lead to recurrence. (3) Incomplete ligation of the pulmonary vessels can cause fatal hemorrhage. (4) Bronchial stump leakage can lead to pneumothorax; always test for air leaks. (5) Overlooking the possibility of multiple lobe torsion; always inspect all lobes during surgery. (6) Inadequate postoperative pain management can lead to respiratory complications.

Perioperative drug protocols for lung lobe torsion are based on Plumb's Veterinary Drug Handbook and current veterinary guidelines. Preoperative stabilization: (1) Oxygen supplementation: 40-60% inspired oxygen via nasal cannula or oxygen cage. (2) Fluid therapy: Balanced crystalloids (e.g., Lactated Ringer's solution) at a rate of 10-20 mL/kg/h for shock, then adjusted based on patient status. (3) Analgesia: Opioids are the mainstay for acute pain. Options include: hydromorphone 0.05-0.1 mg/kg IV q4-6h; fentanyl CRI 2-5 mcg/kg/h; morphine 0.5-1 mg/kg IM or SC q4-6h. (4) Antibiotics: If there is evidence of infection or necrosis, administer broad-spectrum antibiotics: ampicillin 22 mg/kg IV q8h, and enrofloxacin 10 mg/kg IV q24h, or cefazolin 22 mg/kg IV q8h. Intraoperative: (1) Continue fentanyl CRI or add a local anesthetic block (e.g., intercostal nerve block with bupivacaine 1-2 mg/kg, or lidocaine 2 mg/kg). (2) Consider a constant rate infusion (CRI) of lidocaine (25-50 mcg/kg/min) and ketamine (0.1-0.5 mg/kg/h) for multimodal analgesia. Postoperative: (1) Continue opioids for 12-24 hours, then transition to oral opioids (e.g., tramadol 2-5 mg/kg PO q8-12h) or NSAIDs. (2) NSAIDs: carprofen 2.2 mg/kg PO q12h, or meloxicam 0.1 mg/kg PO q24h, or deracoxib 1-2 mg/kg PO q24h. (3) Antibiotics: continue for 7-10 days. (4) If chylothorax is present, consider octreotide 1-2 mcg/kg SC q8h, or a low-fat diet. (5) Gastroprotectants: omeprazole 1 mg/kg PO q12h, or famotidine 0.5-1 mg/kg PO q12h, to prevent stress ulcers. (6) Antiemetics: maropitant 1 mg/kg SC q24h, if needed. (7) In cases of SIRS or DIC, consider low-dose aspirin (0.5 mg/kg PO q24h) or clopidogrel (1-2 mg/kg PO q24h) for antiplatelet effects, but use with caution.

The veterinary literature on lung lobe torsion is limited to case reports and retrospective studies. A landmark retrospective study by Murphy et al. (2017) in the Journal of the American Veterinary Medical Association (JAVMA) reviewed 32 dogs with lung lobe torsion. The study found that the right middle lobe was most commonly affected (50%), and 53% of dogs had concurrent pleural effusion. The survival rate for dogs undergoing lobectomy was 84%. The study concluded that early surgical intervention is associated with a good prognosis. Another study by Park et al. (2018) in Veterinary Surgery evaluated the use of CT in diagnosing lung lobe torsion and found that CT had a sensitivity of 100% and specificity of 96%, making it the imaging modality of choice. A case series by Kim et al. (2020) in the Journal of Veterinary Medical Science reported on 5 cats with lung lobe torsion, all of which were successfully treated with lobectomy, suggesting that the condition is rare but treatable in cats. Consensus guidelines from the American College of Veterinary Surgeons (ACVS) recommend that any patient with suspected lung lobe torsion should undergo immediate thoracic imaging (CT if available) and surgical exploration if the diagnosis is confirmed or highly suspected. The use of thoracoscopic lobectomy has been described in a few case reports and may be an option in stable patients, but open thoracotomy remains the standard of care. Overall, the evidence supports prompt surgical intervention as the definitive treatment, with a favorable prognosis in the absence of severe systemic complications.