Blast injuries seen in various accidents involving pressurized containers like gas cylinders, tires, et cetera, and acts of terrorism. The associated factors can vary from poor handling of equipment to inadequate safety precautions. These injuries include a variety of injuries, such as, injuries due to shock wave, burns, fractures, et cetera, involving multi-organ systems, especially lungs and hollow organs, due to the high-pressurized shock wave. The presented case is of the death of a 24-years-old male as a result of a blast of the compressor present in the AC outdoor unit during the filling of the gas. Here, the body showed injuries due to shock wave, secondary impact, tertiary impact because of fall on the ground, and quaternary injuries due to burns. The cause of death was Blast lung associated with Subarachnoid hemorrhage.

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Traumatic subarachnoid hemorrhage (SAH) is a common finding following traumatic brain injury. In some cases, it can be associated with hydrocephalus. This type of hemorrhage is mostly caused by the rupture of small vessels in the brain and is usually managed conservatively.
We present a case of a 60-year-old woman who presented with traumatic luxation of the eye following a fall. This resulted in diffuse SAH (Fisher grade IV) with associated hydrocephalus. We also report on 3 previous similar cases found in the literature. Avulsion of the ophthalmic artery was found to be the cause of the traumatic SAH. Apart from cerebrospinal fluid diversion using an external ventricular drain, the case was managed conservatively. There was no evidence of delayed clinical or radiologic vasospasm.
Traumatic avulsion of the ophthalmic artery may result in diffuse SAH, mimicking that of aneurysmal rupture. This case shows that management of early complications, such as hydrocephalus and seizures, should be the main aim. Surgical or endovascular treatment of the injured artery, however, would be unnecessary.

Patients with mechanical heart valves are at high thrombotic risk and require warfarin. Among those developing intracranial hemorrhage, limited data are available to guide clinicians with antithrombotic reinitiation. This 13-patient case series of warfarin-associated intracranial hemorrhages found the time to reinitiate antithrombotic therapy (17 days, interquartile range 21.5 days), and changes to international normalized ratio targets were variable and neither correlated with the type, location, or etiology of bleed, nor the valve and associated thromboembolic risk. The initial presentation significantly impacted prognosis, and diligent assessment and follow-up may support positive long-term outcomes.

BACKGROUND: Intracranial pseudoaneurysm is a rare entity, with few cases described in the literature, and is mostly associated with a history of traumatic brain injury. Traumatic aneurysms comprise <1% of all intracranial aneurysms. In particular, middle meningeal artery (MMA) aneurysms are uncommon and usually caused by a skull fracture in the temporal region. About 40 traumatic MMA aneurysms are reported in the literature, and only 28 nontraumatic aneurysms are reported, usually related to high-flow conditions. The behavior of these aneurysms is largely unknown: both spontaneous resolution and aneurysm growth, leading to subsequent rupture, have been reported. Surgical and endovascular management are feasible for MMA aneurysms; however, the criterion standard treatment is not defined.
METHODS: We report the case of a traumatic pseudoaneurysm of the right MMA treated with an endovascular approach and provide a review of the literature.
CONCLUSIONS: Aneurysms of the MMA are a rare entity that must be taken into account in the setting of a traumatic brain injury or predisposing factors. The diagnosis and aggressive treatment are mandatory, preventing the devastating consequences of their rupture. Endovascular and surgical techniques are well defined and available, even though there is not a demonstrated superiority in any of them.

Although strangulation is generally homicidal, the scientific literature reports several cases in which it is suicidal or even accidental. The former eventuality is particularly interesting because extremely atypical ligatures (such as locks of hair), complex dynamics, and uncommon findings can be involved. Only a meticulous evaluation of the body and of both direct and circumstantial evidence can help in the complex differential diagnosis that includes murder, suicide, and accident. In accidental strangulation, the number and severity of injuries depend on the magnitude of applied force. This implies that high-energy strangulation (in our case, caused by the entanglement of a scarf in an electrical generator) can produce a complex polytrauma. In this case, accidental self-strangulation caused widespread, posttraumatic subarachnoid hemorrhaging, laceration of the larynx, and fracture-dislocation of the C2/C3 vertebrae. We believe that all these events contributed to the death of the victim, but the complexity of the polytrauma and the lack of direct evidence did not allow us to determine a univocal cause-effect chain.

BACKGROUND: Cortical ischemic lesions represent the predominant pathomorphological pattern of focal lesions after aneurysmal subarachnoid hemorrhage (aSAH). Autopsy studies suggest that they occur adjacent to subarachnoid blood and are related to spasm of small cortical rather than proximal arteries. Recent clinical monitoring studies showed that cortical spreading depolarizations, which induce cortical arterial spasms, are involved in lesion development. If subarachnoid blood induces adjacent cortical lesions, it would be expected that (i) they also develop after traumatic subarachnoid hemorrhage (tSAH), and (ii) lesions after tSAH can occur in absence of angiographic vasospasm, as was found for aSAH.
METHODS: An 86-year-old woman was admitted to our hospital with fluctuating consciousness after hitting her head during a fall. The initial computed tomography (CT) was significant for tSAH in cortical sulci. On day 8, the patient experienced a secondary neurological deterioration with reduced consciousness and global aphasia. Whereas the CT scan on day 9 was still unremarkable, magnetic resonance imaging (MRI) on day 10 revealed new cortical laminar infarcts adjacent to sulcal blood clots. Proximal vasospasm was ruled out using MR and CT angiography and Doppler sonography. CT on day 14 confirmed the delayed infarcts.
CONCLUSIONS: We describe a case of delayed cortical infarcts around sulcal blood clots after tSAH in the absence of proximal vasospasm, similar to results found previously for aSAH. As for aSAH, this case suggests that assessment of angiographic vasospasm is not sufficient to screen for risk of delayed infarcts after tSAH. Electrocorticography is suggested as a complementary method to monitor the hypothesized mechanism of spreading depolarizations.

Fatal subarachnoid hemorrhage (SAH) caused by anterior communicating artery (ACoA) rupture is a rare event in medicolegal practice. Anatomical variations of the ACoA tend to make its anatomical structure, and as a result, blood flow through it, more complicated, which may increase hemodynamic stress and cause weak spots in the affected blood vessels. Variant ACoAs are prone to rupture in the event of a blunt-force trauma. Here, we report a fatal case of SAH caused by the rupture of a variant ACoA when the victim\'s head was struck from behind, causing the head to rotate and the victim to fall forward onto the ground. A medicolegal autopsy revealed diffuse basal SAH and ACoA duplication. The smaller of the two variant ACoA branches had ruptured near its junction with the right anterior cerebral artery. No basal aneurysms or other fatal diseases or injuries were found. This case highlights the significance of anatomical variation in forensic pathology.

Vertebral artery laceration/dissection (VALD) resulting in fatal subarachnoid hemorrhage (SAH) is a rare, but well-known phenomenon encountered in the forensic setting. Delayed ruptures are exceptionally rare, and pose several challenges to the forensic pathologist. In this paper we present a case of a 47-year-old male who collapsed suddenly following recent complaints of a headache and a reported seizure. He had a reported history of potential head trauma that occurred several days prior. Attempts at resuscitation were unsuccessful, and an autopsy examination was ordered. Computer tomography (CT), autopsy, histological and ancillary studies were performed. External examination showed mild, healing trauma to the head and upper limbs, and pre-autopsy CT demonstrated a SAH. Examination of the brain showed basally oriented SAH, and there was a laceration of the left vertebral artery. Histological examination demonstrated a delayed rupture, and there was no significant blood vessel abnormality. Molecular testing was negative for collagen vascular disorders. Delayed rupture of the vertebral arteries following head trauma is rare. The presence of remote and/or mild trauma may be difficult to establish at autopsy, and it is important to identify underlying aortopathies. Several autopsy techniques and ancillary studies should be performed in these cases.

We present a case of ophthalmic artery (OA) traumatic avulsion, leading to a post-traumatic subarachnoid hemorrhage (SAH) with ventricular blood invasion and hydrocephalus, mimicking an internal carotid aneurysm rupture. This is the third case of such an event reported in literature and the first without orbital fractures and optic nerve avulsion. Conservative treatment was sufficient for the avulsion, but surgery was needed for the coexisting eye luxation. Traumatic OA avulsion is a rare but possible event and should be suspected in case of basal cisterns SAH, evidence of orbital trauma and CT angiogram or angiographic absence of opacification of the OA.