Most (85%) diaphragmatic hernias are a result of trauma. However, not all patients have a history of trauma, nor do they always present with respiratory symptoms. The diagnosis is usually straight forward for those with a history of trauma and respiratory compromise, however, it is not uncommon that a patient will present signs such as chronic weight loss, gastrointestinal signs or symptoms related to a hepatopathy or other organ dysfunction.
Trauma may have taken place months or years prior, unbeknownst to the owner. The hernia can also be an incidental finding during imaging performed for seemingly unrelated reasons.
In cases of acute traumatic herniation, the time to address the hernia should be carefully considered. Rapid control of the airway and ventilation must be weighed against the value of further patient stabilization. Stabilization over several hours to days prior to intervention may be prudent to minimize anaesthetic and surgical risk. The trauma that has resulted in the hernia has very often caused other injuries. Attempts should be made to resolve hemodynamic instability prior to anaesthesia and surgical intervention. An otherwise stable patient is much more likely to survive the repair. In cases of chronic herniation without decompensation the surgery can be scheduled at the surgeon’s convenience.
Ventilation must be provided following anaesthetic induction in all cases of diaphragmatic hernia. The pleuroperitoneal pressure gradient has been abolished and respiratory attempts under anaesthesia will be particularly ineffective. Most anaesthetics impair respiration to some extent and as such decompensation following induction is possible without adequate support. ETCO2 should be monitored throughout these procedures to ensure ventilation is adequate. Inspiratory pressures should be initially limited to 10 or 15 cm of water but increased up to (but not beyond) 20 cm of water as needed. A typical starting ventilation rate of 6–8 breaths per minute is recommended and adjusted accordingly based on ETCO2.
Once the abdomen has been entered, both sides of the diaphragm should be evaluated. It is not uncommon to have multiple hernias or tears. Circumferential and radial tears of the musculature generally predominate. The falciform fat and liver are most frequently herniated, however, the small intestine, stomach, spleen, omentum, pancreas, colon, cecum and uterus can also be herniated. Gentle traction on the herniated organs usually facilitates reduction, however, chronic hernias can have significant thoracic adhesions. Acute herniations surgically managed within 10 days will not have had time to develop adhesions and reduction is often straight forward. However, even acute hernias can be difficult due to congested and friable splenic or hepatic tissue. Torsed vascular pedicles should be noted and de-rotated under controlled circumstances as appropriate or excised if this appears safer. In cases of chronic herniation with extensive adhesions visualization of structures from the thoracic cavity can improve safety. The surgeon should be prepared to perform a caudal sternotomy as required.
During reduction of the hernia the free volume within the thoracic cavity will increase and available volume in the abdominal cavity will decrease. In acute herniations this is generally of less consequence. Care should be taken to evacuate the chest very slowly such that the lungs are not placed under excessive strain. Aggressive ventilation beyond 20 cm of water to re-expand the lungs should be avoided. Negative pressure in the pleural space will facilitate re-expansion of the lungs more slowly and safely. Re-expansion injury can occur in chronic and acute cases secondary to mechanical and reperfusion injury. All efforts should be made to re-expand the lungs slowly. The increased abdominal contents may cause a ‘loss of domain’ necessitating emptying of the bladder, removal of falciform fat and omentum, and even removal of the spleen should this appear to be contributing significantly. Tension relief of the abdominal wall or an expanded closure with a graft is also a potential option. In cases with abdominal tension an indwelling urinary catheter should be placed to allow post-operative measurement of intra-abdominal pressure.
The closure of the diaphragm itself can be performed with synthetic monofilament typically between 3-0 and 0 USP. Suture patterns vary but include simple interrupted, mattress, cruciate, simple continuous patterns (the latter leaving less knot ends that could lacerate hepatic parenchyma). Suturing is generally started dorsally and completed ventrally. Prior to placing the last 1–2 sutures a chest tube can be advanced through the defect and into the thorax. This can then be used to gently remove air from the thoracic cavity with caution not to inflict excessive re-expansion trauma. This tube can then often be removed. In cases where ongoing fluid or gas accumulation are anticipated an indwelling chest tube can be placed.
Post-operative monitoring should include careful evaluation of respiration and blood gas analysis where possible. Adequate analgesia and supportive care provided, the extent of which to be determined on a case by case basis. Abdominal pressures should be below 10 mm Hg, with medial or surgical interventions required beyond this pressure.
Potential complications include pneumothorax, haemothorax, pulmonary re-expansion injury, or other sequelae arising from the original trauma. Post-operative reflux and oesophageal ulceration is seen in some cases. Extended medical management for reflux can become necessary. Although the recurrence rate is generally low, the client should be instructed to monitor closely, and re-evaluation/imaging performed as needed.