Cardiac tamponade, blunt aortic injury and diaphragmatic

• Cardiac tamponade is an emergency in which fluid under pressure fills the pericardium and stops the heart from filling. In trauma it is usually blood (haemopericardium) from a torn chamber, and it kills by obstruction, not by bleeding out.
• Blunt cardiac injury runs from silent contusion to chamber rupture. Most people with a ruptured chamber never reach hospital; the rare survivor needs the tamponade relieved surgically within minutes.
• Blunt thoracic aortic injury is graded I to IV by the SVS system. Grade I is usually watched. Grade II is often manageable without operation in stable patients, while grades III and IV need repair, with the severe injuries done immediately and even stable lesions repaired within 24 hours. When anatomy allows, stent grafting (TEVAR) is preferred to open surgery.
• A traumatic diaphragmatic tear does not heal. It is usually found with other injuries, more often on the left, and an acute rupture should be repaired at the time of the first operation.
• Three major societies guide this page: ATLS for the trauma survey, the EAST Practice Management Guidelines (2012 for blunt cardiac injury screening, 2015 for emergency department thoracotomy), and the Society for Vascular Surgery guideline of 2011 for aortic injury, as summarised in current reviews.

By the end of this page you should be able to:

1. Explain cardiac tamponade from physiology to signs, and judge when Beck triad is present or absent.
2. Compare blunt and penetrating cardiac injury and plan the investigations that rule out or confirm each.
3. State the indications, expected benefit and limits of pericardiocentesis, pericardial window, and resuscitative thoracotomy.
4. Grade a blunt aortic injury and choose between anti-impulse therapy, TEVAR, open repair and surveillance.
5. Recognise a diaphragmatic rupture, know its imaging limitations and operative approach.
6. Apply the ATLS, EAST and SVS recommendations above to a trauma patient.

This page covers four life-threatening injuries of the thorax that share one feature: they are easy to miss while the patient is bleeding or breathless, and they are reversible only if sought early. They often travel together after high-energy trauma, and each has its own decision point. Cardiac tamponade is relieved by drainage and then by suture. Blunt aortic injury is staged and either watched, repaired early or repaired now. Diaphragmatic rupture is repaired in the same operation that fixes everything else. The unifying theme is the primary survey: nothing here is found if you do not look for it.

A cardiac tamponade is a pericardial syndrome in which fluid accumulates under pressure and impairs diastolic filling until cardiac output falls. In trauma the fluid is usually blood. The diagnosis is clinical: it requires both a pericardial effusion and haemodynamic instability.^[4]

Cardiac injury is classified by mechanism. Blunt cardiac injury (BCI) is damage to the heart from non-penetrating trauma, ranging from a contusion that needs only monitoring to free-wall rupture. Penetrating cardiac injury (PCI) is a stab wound or missile tract that breaches the myocardium; it may produce tamponade (if the wound seals and blood stays in the pericardium) or exsanguination (if it decompresses into the pleura).^[1][5]

Blunt thoracic aortic injury (BTAI) is an injury to the thoracic aorta from blunt force, commonly graded I to IV: grade I is an intimal tear, grade II an intramural haematoma, grade III a pseudoaneurysm and grade IV free rupture.^[6]

Traumatic diaphragmatic rupture (TDR) is disruption of the diaphragm from blunt or penetrating thoraco-abdominal trauma, with or without herniation of abdominal viscera. It does not heal spontaneously because the diaphragm moves with every breath.^[7]

BCI follows most often from motor vehicle collisions with rapid deceleration; a direct blow to the precordium and a raised abdominal pressure at impact also account for many cases. Of diagnosed BCIs, cardiac contusion is the most common, and the right heart is the most often injured because it lies closest to the sternum. Most patients with a ruptured chamber die at the scene; the incidence of BCI in blunt chest trauma overall is unknown because there is no single accepted definition.^[1]

Penetrating cardiac injury is rare but lethal. In one decade of a level 1 trauma centre, 406 of 40,706 trauma admissions (1.0%) sustained a penetrating cardiac injury; only 109 (26.9%) survived to discharge. The survivors were predominantly male (94.4%), averaged 30.8 years of age, and 74.3% had sustained a stab wound. The right ventricle was the most often injured chamber, followed by the left ventricle.^{[5] [3]}

Traumatic diaphragmatic rupture occurs in about 0.4 to 0.5% of all trauma patients. Around 80% are left-sided, because the liver protects the right hemidiaphragm, and only about 2% are bilateral. On average, TDR is now more often caused by penetrating trauma (63%) than by blunt injury (37%). Among blunt trauma cases the incidence is higher (about 1.9%), and more patients are initially detected. Among patients with trauma, diaphragmatic injury is clinically found far more often on the left, although autopsy studies see left and right injuries equally often. Blunt TDR carried a hospital mortality of 15% in one multicentre series, versus 4% for penetrating TDR.^[7]

BTAI occurs in an estimated 1 to 2% of level 1 and 2 trauma patients, usually within motor vehicle collisions. It accounts for 16% of deaths after motor vehicle collision, second only to head injury, and as many as 80 to 90% of cases are immediately fatal before arrival at hospital. For those who survive to reach a trauma centre, prompt detection decides outcome.^[6]

BCI is produced by a small set of mechanisms: rapid deceleration with the heart thrown against the sternum, compression of the heart between sternum and spine, abrupt intrathoracic and intra-abdominal pressure spikes, shearing, blast and crush. A sternal fracture raises the suspicion markedly: in one autopsy series sternal fractures were found in 76% of fatal cases with cardiac injury but only 18% of deaths without BCI. A sternal fracture on its own, however, neither proves nor predicts BCI.^[1]

Penetrating cardiac injury follows whatever wounds the precordium; cardiac rhythm, haemodynamics and the size of the pericardial defect then decide whether tamponade or exsanguination results. Long, sharp knives and low-velocity stab wounds are the mechanism most often survived; gunshot wounds carry far lower survival.^[5]

BTAI mechanisms are deceleration and osseous pinch. A change of velocity of more than 20 miles per hour combined with passenger-compartment intrusion above 15 inches is a recognised risk factor, and lateral impact collisions carry higher mortality than head-on impacts. Haemodynamically, the "water-hammer" effect is thought to generate pressures over 2000 mmHg at the aortic arch. Most injuries occur at the isthmus, a few centimetres distal to the origin of the left subclavian artery, where the relatively mobile arch meets the fixed descending segment.^[6]

Diaphragmatic rupture is produced by a sudden large rise in intra-abdominal pressure, an estimated ten-fold increase during severe abdominal trauma, acting across a pressure gradient of 7 to 20 cm of water between abdomen and pleura. The left side tears more often because the diaphragm is weaker there embryologically and is not cushioned by the liver. Blunt causes include decelerating motor vehicle collisions, falls from height and crush of the lower chest and upper abdomen. Penetrating causes are stab and gunshot wounds of the thoraco-abdominal zone. Iatrogenic, pregnancy-related and unexplained spontaneous ruptures are recognised but uncommon.^[7]

Tamponade begins with the pericardium's compliance. It stretches slowly, so up to 1000 mL of fluid may accumulate over time without haemodynamic effect. Rapidly accumulating blood, as little as 150 mL, can raise pericardial pressure steeply and abolish cardiac output. Once the elastic limit is reached, pericardial pressure dictates filling pressure of the chambers; equalisation of right and left atrial and ventricular diastolic pressures to roughly 20 to 25 mmHg is typical. The right atrium and right ventricle collapse in early diastole, systemic venous return falls, the septum shifts left and pulsus paradoxus appears. Tachycardia is the first compensatory response and it is often inadequate. Ventilation is hazardous because positive pressure reduces venous return further. External chest compression has little value because there is almost no room for additional filling.^[4]

Blunt cardiac injury spans myocardial contusion, valvular and septal disruption, and free-wall and atrial rupture. Contusion of the right ventricle against the sternum produces arrhythmias (right bundle branch block especially) and enzyme release. Most free-wall ruptures are instantly fatal; survival requires the rupture to be small, low-pressure (usually atrial, at the junction of the atrium with the vena cava or pulmonary veins), tamponaded by pericardium, or decompressed through a pericardial tear into the pleural space as a massive haemothorax. Survival in reported surgical series of contained rupture ranges from 39 to 100%, depending on the degree of preoperative instability. Tamponade from an atrial tear is sometimes controlled by needle or catheter drainage until repair, whereas haemorrhage from a ventricular tear usually needs emergency department thoracotomy because pericardiocentesis may not keep up with bleeding.^[1]

Penetrating cardiac injury follows the same tamponade physiology but with two twists. The sudden compression usually comes from a small knife wound that seals after impact, generating tamponade that can keep the patient alive to hospital. A large or jagged wound allows decompression into the pleura, producing a haemothorax and rapid exsanguination with no tamponade. This is why the absence of a pericardial effusion on ultrasound does not exclude serious cardiac injury in a haemodynamically compromised patient.^[1][5]

BTAI runs from a small intimal flap (grade I) through intramural haematoma (grade II) and pseudoaneurysm (grade III) to free rupture (grade IV). The lesion is partly sealed by adventitia and mediastinal tissues until repair. Severe injuries (grades III and IV) can rupture at any time, which is why anti-impulse therapy is begun immediately and definitive repair is not delayed once the patient is stabilised.^[6]

Diaphragmatic injury matters because the pressure gradient works against the patient forever: abdominal viscera herniate through a defect that enlarges rather than heals, producing mediastinal shift, lung compression, obstruction or strangulation years later. In the acute phase the associated abdominal and thoracic injuries decide survival.^[7]

Beck triad comprises hypotension, elevated jugular venous pressure and muffled heart sounds, with tachycardia and pulsus paradoxus (an inspiratory fall in systolic blood pressure above 10 mmHg) as supportive findings. Other clinical findings may include tachypnoea, cool peripheries and electrical alternans with low QRS voltage on the electrocardiogram.^[4]

The challenge is that trauma rarely presents the classic picture. After injury the patient may be hypovolaemic rather than venously congested, neck veins may not be distended and heart sounds are hard to hear in a noisy resuscitation bay. Distended neck veins and muffled sounds can be absent when shock is haemorrhagic. The ECG voltage may be normal. In practice, tamponade in trauma is suspected when hypotension is out of proportion to estimated blood loss or does not respond to fluid, when there is a wound in the "cardiac box" or when chest radiograph or physiology suggest a compressive cause, and it is confirmed at the bedside by ultrasound.^[1][4]

Symptoms range from none to chest soreness, dyspnoea and collapse. The right ventricle is closest to the sternum, so arrhythmias (particularly right bundle branch block) and contusion of the right ventricle are the typical patterns. New electrocardiographic abnormality, persistent arrhythmia or unexplained hypotension after sternal or high-energy chest trauma should make you suspect BCI. Septal, valvular and coronary artery injuries are uncommon but present with acute valve regurgitation, a new murmur or haemodynamic failure from ischemia. Late presentations include congestive heart failure from longstanding valve dysfunction.^[1]

Stab and gunshot wounds are the usual mechanism. In the largest registry, signs of life were present on admission in 92.6% of patients, which explains why prompt aggression saves people. The clinical picture is either tamponade (hypotension, raised jugular venous pressure, muffled sounds, perhaps a wound over the precordium) or exsanguination (haemothorax, massive external bleeding, signs of shock without a venous pressure rise). A small knife wound can stop bleeding into the pericardium and sustain life; a larger wound does not.^[5]

Survivors most often complain of retrosternal chest pain and dyspnoea. Other symptoms include cough, referred inter-scapular pain and hoarseness. On examination, hypotension, a pulse deficit between arms, upper-limb hypertension and visible chest-wall injury are classic clues. The initial chest radiograph is useful but unreliable: common findings include mediastinal widening of 8 cm or more or 25% of thoracic width, loss of aortic contour and tracheal deviation, yet up to 7% of radiographs are read as normal despite an injury. Therefore, CT angiography is first-line imaging whenever the presentation raises concern.^[6]

In the acute phase patients have abdominal and chest pain with cardio-respiratory compromise; findings are often dominated by the associated injuries (head injury, liver or spleen laceration, multiple rib fractures). An acute left hemidiaphragm tear may show itself radiographically by herniated stomach, colon or omentum; bowel sounds in the chest are a telling sign. In the latent phase, symptoms are vague upper gastrointestinal complaints, chest or left upper quadrant pain, dyspnoea or orthopnoea, followed in the obstructive phase by progressive symptoms and signs of incarceration. Right-sided ruptures are harder to spot and can mimic liver or lung pathology.^[7]

Differential diagnosis for thoracic trauma with hypotension has three principal categories, and sorting them before acting is the hardest part.

For BTAI, the main imitator on imaging is a ductus diverticulum (wide base, smooth margins, obtuse angles, usually with no periaortic haematoma) and an infundibulum at a brachiocephalic origin. A mediastinal haematoma without periaortic involvement usually has another source.^[6]

For diaphragmatic rupture, the differential includes phrenic nerve palsy, eventration, congenital hernia and normal variant of a raised hemidiaphragm; in trauma, always assume rupture with an elevated diaphragm until proven otherwise after high energy.^[7]

Bedside echocardiography is the investigation of choice. It is fast, needs no patient movement and serves both diagnosis and treatment. A large effusion is an easy call; a small, loculated haemopericardium in a pericardial tear is not, and TEE or CT may be needed. The ECG is useful (low voltage, electrical alternans) but not sensitive, and the chest radiograph is normal until at least a moderate effusion. In acute traumatic tamponade, rapidly accumulating pericardial blood, as little as 150 mL, may produce collapse.^[4]

FAST and eFAST are the trauma versions. They detect pericardial fluid early, guide pericardiocentesis and allow serial checks after blunt trauma. For cardiac tamponade, echocardiography shows right atrial and right ventricular diastolic collapse, a dilated non-collapsing inferior vena cava and marked respiratory variation of mitral and tricuspid inflow.^[4]

The EAST 2012 practice management guideline sets a clear, defensible algorithm.^[2]

• Level 1: an admission electrocardiogram should be performed in every patient in whom BCI is suspected.
• Level 2: if the ECG is normal and troponin I is normal, BCI is ruled out (the optimal timing of these tests is not yet determined). A new ECG abnormality of any kind warrants monitoring. Patients with normal ECG but elevated troponin I should be monitored. Echocardiography is reserved for patients with haemodynamic instability or persistent new arrhythmia, via the transthoracic route and transoesophageal route if the transthoracic study is inadequate. A sternal fracture on its own should not prompt monitoring when the ECG and troponin I are normal. Creatine kinase isoenzymes are not useful and nuclear medicine studies add little compared with echocardiography. ^[2]
• Level 3: troponin I should be measured routinely in suspected BCI; if raised, the patient should be monitored with serial testing, though the optimal interval is unknown. CT or MRI can help separate acute myocardial infarction from BCI.

A 12-lead ECG is also widely used in the ATLS approach: look specifically for arrhythmias, ST changes, heart block and unexplained ST abnormalities, and monitor continuously if any of these appear. Echocardiography establishes structure (wall motion, valve function, tamponade, septal or free-wall rupture) and magnetic resonance gives the best tissue characterisation, including differentiating contusion from ischaemia.^[1][2]

In the stable patient with a wound near the heart, transthoracic echo (or CT) looks for haemopericardium. Subxiphoid pericardial window is a bedside diagnostic tool with a long track record; when a CT chest is done in a stable patient, pericardial fluid can be seen directly. Anatomical disagreements are settled in theatre. The practical rule is that a patient with a wound of the precordium and instability goes to the operating theatre, not to the CT scanner.^[5]

CT angiography of the chest and abdomen is the first-line and decisive test, with sensitivity approaching 100% and specificity above 80%. Multiplanar reconstructions are essential, and the sagittal plane lets you run the eye along the aorta. Direct signs (pseudoaneurysm, focal contour abnormality, intimal flap, intramural haematoma, abrupt calibre change, contrast extravasation) are highly specific; indirect signs include mediastinal haematoma with periaortic involvement. When the diagnosis is still equivocal in a stable patient, transoesophageal echo approaches 97% sensitivity and specificity, and intravascular ultrasound at the time of repair helps size the graft because CTA often underestimates aortic diameter in young trauma patients. Invasive catheter angiography is now usually a planning tool rather than a diagnostic one.^[6]

Chest radiography is the first, simplest test but it diagnoses or suggests the rupture in only 25 to 70% of cases. Helical CT sensitivity for left-sided rupture is 78% and right-sided 50%; multidetector CT reaches specificity of 100% on the left and 83% on the right. The diagnosis can be supported by an elevated or irregular diaphragm, non-visualization of the diaphragmatic edge, herniated abdominal contents, mediastinal shift without lung cause, and compression atelectasis of the lower lobe. MRI is best for latent or chronic hernias but is impractical in polytrauma. In practice, a very high index of suspicion and direct visualisation at laparoscopy or thoracoscopy settle the diagnosis in borderline cases; in selective non-operative management of penetrating thoraco-abdominal trauma, a diagnostic laparoscopy at 48 hours has found a diaphragmatic injury in 22% of patients with a left stab wound.^[7]

BTAI is graded by severity, I to IV as above. Grade I is usually managed expectantly, and many grade II (minimal) injuries are now managed without operation in stable patients; grades III and IV require operative repair. Initial management for any grade is large-bore access, intensive-care monitoring and anti-impulse therapy (stricter blood pressure and heart rate control, with systolic pressure under 100 mmHg and heart rate under 100 beats per minute) while the definitive decision is made. Severe injuries (grades III and IV) should be repaired immediately; grade II injuries can be delayed beyond 24 hours if anti-impulse therapy is instituted and there is no evidence of progression. All haemodynamically unstable patients with suspected or proven injury go to a hybrid operating room for immediate treatment. Older SVS guidance (as summarised in current reviews) advises that when repair is required it should take place within 24 hours of injury, whereas the 2026 SVS focused update suggests delayed TEVAR beyond 24 hours in haemodynamically stable grade 3 injuries, and urgent or emergent repair when the aortic injury itself causes instability. ^{[6] [9]}

Severity scoring for diaphragmatic injury is by the AAST scale (grade I contusion to grade V tissue loss). In the acute phase the score matters less than the associated organ injuries.^[7]

The initial survey follows the ATLS sequence. In shock, search for tamponade alongside haemorrhage, because the distinction changes treatment. The 9th edition ATLS manual, as cited by the diaphragmatic-injury literature, prescribes the same primary survey and secondary survey structure.^[7]

If pericardial fluid is found on ultrasound and the patient is hypotensive or in shock, pericardiocentesis is performed immediately. Echo-guided or fluoroscopy-guided needling is the preferred route, because imaging shows the needle tip and allows the shortest, safest path. In loculated collections, especially clotted haemopericardium, needle drainage is often inadequate; open surgical drainage gives the chance to control the bleeding source. Pericardiocentesis can be followed by a drainage catheter and interval definitive repair. Intravenous fluid and inotropes may temporise but must not delay or replace drainage; mechanical ventilation should be avoided if possible because it lowers cardiac output further; external cardiac compression has little value in tamponade.^[4]

For atrial tears, repeated drainage with a pig-tail catheter until definitive repair can work. For ventricular tears and unstable patients, drainage does not keep pace and emergency department thoracotomy is preferred.^[1]

Resuscitative thoracotomy (RT) is the primary-survey act of opening the chest to relieve tamponade, control thoracic haemorrhage, open cardiac massage and cross-clamp the aorta. It is a salvage procedure, and selection matters more than technique. The EAST 2015 practice management guideline on emergency department thoracotomy gives the best current framework.^[3]

• Signs of life present, defined as pupillary response, spontaneous ventilation, a carotid pulse, measurable blood pressure, extremity movement or cardiac electrical activity.
• After penetrating thoracic injury, EAST strongly recommends thoracotomy with signs of life (182 of 853 patients, 21.3% survival) and conditionally recommends it without signs of life (76 of 920 patients, 8.3% survival; among the 641 patients in whom neurological outcome was reported, 25 (3.9%) survived neurologically intact). ^[3]
• After penetrating extrathoracic injury, thoracotomy is conditionally recommended with signs of life (25 of 160, 15.6% survival) and conditionally recommended without signs (4 of 139, 2.9% survival). ^[3]
• After blunt injury, thoracotomy is conditionally recommended with signs of life (21 of 454 patients, 4.6% survival) and conditionally recommended against without signs of life (7 of 995 patients, 0.7% survival; among the 825 patients in whom neurological outcome was reported, only one (0.1%) survived neurologically intact). ^[3]
• Arrest time is a vital component of the decision. The EDT literature is unable to set an exact CPR duration; the commonly held limit is 15 minutes after penetrating injury and essentially none survive longer. The Western Trauma Association offers practical cut-offs for non-recovery: blunt trauma patients with more than 10 minutes of prehospital CPR and no signs of life are pronounced dead; penetrating torso trauma patients with more than 15 minutes of CPR are pronounced. Only 1 to 2% of blunt trauma patients undergoing RT survive overall.^[3][8]

A more recent prehospital cohort found that RT for tamponade improved survival, particularly when performed within 10 minutes of arrest, but prehospital RT is a specialist service and not a general model of care. Where resources are limited, the principle is the same: open the pericardium as fast as possible by the safest available route.^[8]

Unstable patients with a precordial wound go straight to thoracotomy or sternotomy; stable patients are imaged first. Operative steps are pericardial opening (often best long and off to the side of the phrenic nerve), digital control of the wound, then mattress sutures under the fingers, with care around coronary vessels, using pledgets where the tissue is soft. Definitive repair follows. After repair, screen for intracardiac injuries (septal defect, valve injury) with echocardiography before discharge, because these are found in a meaningful minority and usually need no further operation. Follow-up echocardiography is warranted: in one large series, 26.9% survived to discharge, almost half the survivors had an abnormal echo, yet most complications needed no operation. Recovery without anticoagulation is usual for simple muscle repair.^[5]

Pericardiocentesis in PCI deserves a warning: loculated clotted blood makes needle drainage unreliable and can delay life-saving surgery. A pericardial window or direct opening of the chest is preferable when tamponade is suspected and drainage does not improve the patient.^[1]

The first action is anti-impulse therapy, begun in the intensive care unit while images are completed: beta-blockers (negative inotropy) and antihypertensives, aiming for systolic pressure under 100 mmHg and heart rate under 100 beats per minute.^[6]

Grade I injuries are observed, with anti-impulse therapy as the default and surveillance until resolution, because most intimal injuries heal spontaneously. Grade II has traditionally required repair, but modern select series have safely managed many grade II injuries without operation; grades III and IV must be repaired. Repair timing depends on grade and stability: older SVS guidance as summarised in current reviews aims for repair within 24 hours where feasible, whereas the 2026 SVS focused update suggests delayed TEVAR beyond 24 hours for stable grade 3 injuries and urgent or emergent repair when the aortic injury itself causes instability; severe injuries are done immediately or in the hybrid operating room if the patient is unstable. The competing interest of traumatic brain injury, where permissive hypertension may be needed, can make immediate stenting attractive even for lower grades, because a repaired aorta removes the need for strict pressure control. ^{[6] [9]}

When repair is needed, TEVAR is the default in patients with suitable anatomy. It is done through femoral access, with IVUS to improve sizing, landing zones of healthy aorta of roughly 2 cm, proximal landing zone diameter under 42 mm, and care to avoid angulated landing zones. Coverage of the left subclavian is usually well tolerated; revascularise selectively if brain or cord perfusion is threatened. Open repair (clamp-and-sew, left-heart bypass or full cardiopulmonary bypass with heparinisation) is reserved for unfavourable anatomy. Outcomes of TEVAR are materially better than open repair, with lower stroke and spinal cord ischaemia, though endoleak is the commonest late complication; surveillance after TEVAR is institution-specific, with older reviews describing a first check at 1 month and annually thereafter (extending to every 2 years if stable for 2 years), while the 2026 SVS focused update calls for no routine surveillance of stable grade 1 injuries, a single CTA at 1 to 3 months for grade 2 injuries managed non-operatively, and postoperative surveillance after TEVAR. ^{[6] [9]} Open repair still carries a historical mortality and paraplegia burden (up to 28% and 16% in older series).

Aortic-related survival after TEVAR for aortic injury is excellent, and operative mortalities of open repair remain considerably higher. The old SVS 2011 guideline (summarised in current reviews) is still quoted for grade-based management, anti-impulse and TEVAR-first strategy.^[6]

Acute TDR should be repaired during the patient's first operative exploration, because associated life-threatening injuries set the priority and the tear will not heal. A primary repair usually suffices. Small defects up to 5 to 6 cm are closed with interrupted No. 0 or No. 1 monofilament absorbable or non-absorbable sutures. Larger defects need interrupted figure-of-eight or horizontal mattress sutures; some authors use a two-layer closure. Mesh is rarely needed.^[7]

Approach follows the patient, not the injury. Acute injuries are best repaired through a midline laparotomy, which also exposes the abdominal organs, the spleen, the liver and both diaphragms; a transthoracic or thoracoscopic approach is favoured for delayed or chronic tears, and is obligatory on the right because the liver blocks transabdominal access. If during exploration of one cavity an injury is visible through the tear, the defect can be enlarged and repaired through the tear (transdiaphragmatic approach). When the patient needs no abdominal exploration but injury is suspected, diagnostic laparoscopy or thoracoscopy is appropriate, including a check performed 48 hours after admission for a left thoraco-abdominal stab wound.^[7]

Chronic traumatic diaphragmatic hernia must be repaired electively, and urgently if obstruction, incarceration or strangulation develops. The transthoracic route is the usual choice. Once herniation has produced adhesions to lung and chest wall, adhesiolysis and decortication may be needed. Mesh can be used for large chronic defects.^[7]

The practical rules during repair are: reduce the herniated viscera into the abdomen, ensure watertight closure and leave a chest tube in the hemithorax. Pass a small nasogastric tube alongside the herniated organs to avoid gastric distension, and irrigate the haemothorax thoroughly if perforation has contaminated it.^[7]

Tamponade and its treatment carry the usual risks of external compressions and false negatives: missing a clotted collection, a malpositioned needle, injury to a coronary vessel or myocardium, pneumothorax and recurrent effusion. Loculated traumatic effusions are often best handled surgically. Surgical decompression of a tamponade can trigger sudden hypotension from re-expansion, requiring prepared vasopressors.^[4]

Complications of BCI include cardiac failure from contusion, delayed valvular dysfunction, septal defect, myocardial infarction from coronary thrombosis or dissection and sudden death from valve obstruction. After emergency repair of PCI, a significant minority develop an abnormal echocardiogram (pericardial effusion, wall-motion abnormality, reduced ejection fraction, intramural thrombus, valve injury, aneurysm or septal defect), but most need no operation and one-year survival after discharge is about 97%. PCI also carries a high postoperative risk of further complications if undrained collections recur.^[5]

Complications of BTAI include endoleak (up to 15%, type I the most common in trauma), endograft collapse, infection, device failure and migration. Open repair complications include haemorrhage, infection and paraplegia. Asymptomatic patients still need reliable surveillance imaging.^[6]

TDR complications include delayed herniation, incarceration, strangulation, bowel obstruction, empyema, atelectasis and technical failures from missed injury at the first operation. A missed diaphragmatic defect is one of the most serious occult injuries in abdominal trauma.^[7]

The sobering statistic for PCI is that fewer than one in every four patients who reach hospital alive survives to discharge, because the wound is either lethal at scene or too large to seal. For those who reach a hospital with signs of life, resuscitative thoracotomy has a conditional recommendation with a small but real benefit. Blunt cardiac rupture that is contained can be repaired with 39 to 100% survival depending on presentation, but even in experienced centres non-survival at scene is the rule. Diaphragmatic injury itself is rarely fatal unless other injuries dominate; hospital mortality was 15% for blunt and 4% for penetrating TDR in one series, largely from associated damage. BTAI mortality is driven by accompanying injuries and by whether the patient reaches a trauma centre; early diagnosis and TEVAR have lowered it greatly.^[1][5][6][7]

Prevention is mostly road safety: seat belts (which themselves can cause sternal fracture and BCI) lower high-energy mortality, and crush prevention in industry and sport matters for the diaphragm. Screening for BCI uses the ECG-first rule above: an admission ECG in everyone at risk, troponin I to complete the picture, and monitoring only when either is abnormal. Stopping at this low threshold has been shown to be safe.^[1][2]

For PCI and tamponade, there is no screening test beyond awareness of the mechanism; every penetrating wound of the precordium is assumed to involve the heart until imaging or theatre says otherwise. Prevention of diaphragmatic rupture comes down to the same trauma-prevention measures.^[5]

Children. Blunt cardiac injury in children is uncommon but arises from the same mechanisms, and BCI screening principles (ECG, troponin, selective echo) apply at all ages. TDR in children is rare outside high-energy trauma.

Pregnancy. Pregnancy raises the cost of abdominal trauma but does not change the repair principle; delay of repair for fetal reasons is not justified for haemodynamically significant injury.

Older adults and anticoagulated patients. Pericardiocentesis is riskier with coagulopathy, and aspirin or anticoagulants raise the chance of rebleeding from a needle site. Any complex or recurrent collection in this group is better handled by surgical drainage.^[4]

• Many of these patients will be managed where there is no catheter lab, no TEVAR and no immediate cardiothoracic surgeon. The first life-saving steps are all low-tech: ATLS primary survey, early focused bedside ultrasound, chest X-rays, FAST, blood and a clear surgical triage plan.
• A pericardial effusion seen on any ultrasound in a shocked patient justifies immediate needle or open drainage; a subxiphoid pericardial window is a reliable diagnostic and therapeutic procedure if you are not confident blind needling, and it avoids multiple cardiac punctures. Surgical drainage and direct repair are safer where clotted collections are likely.
• For tamponade, external cardiac compression does not help; treat the cause.
• For BTAI without endovascular capability, open repair (or transfer to the nearest centre with the capability) is the only safe route; meanwhile, rigorous anti-impulse control is the bridge, using whatever beta-blockade and vasodilation is available, and accepting less tight control if there is significant brain injury.
• For diaphragmatic rupture, keep clinical suspicion high with high-energy or penetrating thoraco-abdominal trauma. Radiographic clues, an elevated diaphragm, an absent gastric bubble, or bowel loops and air above the diaphragm warrant laparotomy. Primary repair with heavy monofilament suture is achievable in any theatre. If you lack chest tube insertion capability, do not attempt complex thoracic repair without transfer. Inspection of both hemidiaphragms is mandatory at every laparotomy for trauma.^[7]

• Cardiac tamponade kills by impaired filling, not by loss of blood; it needs effusion plus shock.
• Beck triad is hypotension, raised jugular venous pressure and muffled heart sounds; pulsus paradoxus is an inspiratory systolic fall above 10 mmHg; all are insensitive in trauma.
• Treat tamponade by drainage first, then surgery; needle drainage is often insufficient for clotted blood.
• Blunt cardiac injury runs from silent contusion to chamber rupture; contusion is the commonest and is diagnosed by ECG and troponin, with echocardiography reserved for haemodynamic instability or new arrhythmia.
• Penetrating cardiac injury kills by tamponade or exsanguination; the survivors are usually stab wounds with signs of life; after repair, echocardiographic follow-up is worthwhile because most complications need no operation.
• Resuscitative thoracotomy has a real benefit in penetrating injury with signs of life (21.3%), a small benefit without signs (8.3%) and little value after blunt injury without signs (0.7% survivors), none of whom do well neurologically.
• Blunt aortic injury is graded I to IV; anti-impulse therapy comes first (systolic pressure under 100 mmHg, rate under 100), grade I is usually watched, grades III and IV are repaired now, and TEVAR is preferred when anatomy permits.
• Aortic injury is mainly at the isthmus and is imaged best by CT angiography; 7% of initial chest radiographs are normal.
• Diaphragmatic rupture does not heal; left-sided and penetrating causes predominate; chest X-ray detects it in roughly one-quarter to three-quarters of cases, and MDCT is far better on the left than the right.
• Acute diaphragmatic rupture is best repaired through a laparotomy, right-sided and chronic through the chest; primary repair with No. 0 or No. 1 monofilament suture closes most defects.
• Guidelines follow ATLS for the survey, EAST for blunt cardiac injury screening (2012) and resuscitative thoracotomy (2015), and the SVS aortic injury strategy of 2011 as reflected in current reviews.

• Chest trauma and ATLS primary survey
• Pericardiocentesis
• Focused assessment with sonography in trauma (FAST)
• Traumatic aortic injury imaging
• Hemothorax and pneumothorax
• Massive transfusion and trauma resuscitation
• Traumatic cardiac arrest
• Penetrating abdominal trauma
• Intercostal chest drainage

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