Craniocerebral Missile Injuries

Introduction 

Whom to operate? 

Till the turn of the twentieth century, craniocerebral missile injuries (CMIs) were considered uniformly fatal. However, due to the pioneering efforts of people like Sir Victor Horsley followed by the wartime experiences of Harvey Cushing, Donald D. Matson, Geoffrey Jefferson, etc., it was demonstrated that these injuries could be treated with meaningful survival. The degree of brain damage caused by missile is variable. Although no uniformly definite criteria exist for stratification of survivors (with or without disability), certain guidelines can be adhered to. Outcome is closely correlated to patient’s GCS at the time of admission [20,32,47]. Patients who are decerebrate with absent oculocephalic and pupillary reflexes upon admission have a mortality rate of 94 to 97 %, [32] while those who are flaccid have a mortality rate of 100 % [50]. Of the few who survive, the majority will remain vegetative. Hence, those patients with GCS of less than five, decerebration, flaccidity, dilated fixed pupils are not considered for surgery as they rarely survive [13,22,32,56]. In most series, two groups have been described based on correlation of outcome to GCS – those with GCS of 12 to 15, and those with less than 5.46 The former have a good outcome, while the latter have a poor outcome, irrespective of surgery. Patient population with GCS 5 to 12 are the ones who will require early neurosurgical intervention to im­prove outcome, and those who are likely to be benefited by surgery [36,37]. 

There is another subset of patients, who are neurologically intact after CMI. They have only a small uncontaminated puncture wound of entry without evidence of raised ICP, and CT shows no evidence of contusion or extraaxial hematoma, and often a small intracerebral hematoma which does not cause any mass effect and the basal cisterns are well visualised. These patients can be managed conservatively with simple closure of the external wound, administration of appropriate antibiotics for two weeks and follow-up.

While most of the recommendations follow the wartime experience of various neurosurgeons, lessons from various such studies in civilians too can be extrapolated to managing these patients. This review deals with operative management of craniocerebral injury; role of anticonvulsants is not analyzed here.

Principles of Surgery

Overall management can be considered to be a four-tiered approach: 

(a) Immediate life saving measures, such as resuscitation, external hemostasis, splinting of long bone fractures, cerebral decompression, etc. 

(b) Preservation of neural tissue and structures.

(c) Prevention of infection.

(d) Restoration of anatomic barriers against CSF leak and infection.

While there is voluminous literature on military and civilian CMIs, certain aspects have to be kept under consideration while approaching and analyzing these injuries. Most of the military CMIs are sustained from pieces of shrapnel from exploding devices, unlike in civilian injuries, where these are from bullets, often at short range: in suicidal injuries, these are fired at point blank range. Most individuals sustaining high-velocity bullet CMI do not survive. Infection from contamination is more likely in military and battlefield injuries. Lastly, unlike in civilian injuries in developed countries, military CMIs may not reach a neurosurgical centre early enough, terrain and mode of evacuation, battlefield conditions being important factors in evacuation. In developing countries however, many of the civilian CMIs may be delayed due to lack of facilities for evacuation. Hence, surgery may have to be carried out by surgeons who have had little exposure to neurosurgery (especially head injuries), in a zonal or district hospital. It is therefore important that certain facts must be remembered by anyone who ventures to operate on these patients. A general surgeon or a trauma surgeon who operates on such patients should aim at providing immediate decompression and hemostasis, so that the patient can be transported to a neurosurgical center. The basic prerequisites for conducting exploration of a patient with CMI are an adjustable operating table, bright fibreoptic light, high pressure suction, bipolar coagulator and an anesthesiologist capable of maintaining the hemodynamic status as well as cerebral perfusion. 

The overall results of surgery are limited by the pathophysiologic events that accompany CMI. The goals of surgery are thus specific, with aim of reducing the ICP and avoidance of suppurative complications. Broadly, the goals of surgery in CMI can be stated as follows [-52]: 

(a)Evacuation of intracranial hematoma and non-viable brain along the path of the missile

(b)Removal of missile(s) and bone fragment(s) where feasible

(c)Repair and closure of dura and scalp in water-tight fashion

(d)To minimize elevations of ICP in the postoperative period.

Wound debridement & ­operative management

Exposure: Wound should be exposed in the operation theatre. Whole of the scalp is shaved and draped in such a manner that extension of the scalp incision will not be hampered. Head is preferably rested in a ring, since the head position may required to be changed during surgery. Entry site should be debrided. Scalp tags, unless devitalized or tattooed, should be preserved; even free scalp fragments may remain viable and should be preserved. The scalp wound is enlarged by a lazy ‘S’ or ‘Z’ extension. Puncture wounds without any brain matter or CSF leak can be closed and and a formal scalp flap is planned as for a craniotomy. While craniotomy is preferable, craniectomy may have to be done in case of severe communition. Normal dura has to be exposed all around the injury site and opened by radial incisions. Stay sutures are inserted in dura, and all bleeding points are coagulated before dislodging the clot and devitalized brain matter. Dura can be coagulated without hesitation for hemostasis, since closure will have to be made using a dural substitute in practically every case. 

Wound management & hemostasis: Experiences gained in various wars have taught us the benefits of less aggressive approach [11,19,20,24,47,57]. With the availability of CT, the issue of extent of debridement of missile track has undergone a change from radical excision practiced earlier. Devitalized brain, clots and bits of debris are suctioned out and wound is gently irrigated. It is at this point that bleeding usually recommences and has to be tackled simultaneously. Part of the brain which has been debrided should be covered with cotton patties or gelfoam while other parts of the wound are being tackled. Wound is gently irrigated, since forceful irrigation may dissect through the white matter, and should be avoided. Irrigation is done with saline with a soft cannula; touching with metallic cannulae and suction nozzles should be avoided since they can injure the swollen but viable brain. After suctioning away the clot and devitalized brain, attention is directed to bone chips, hair and other foreign bodies which can be picked up with forceps, or can be dislodged with gentle irrigation. Only the obviously devitalized brain should be suctioned out and not the surrounding, swollen brain, which may be viable [6,47,48]. The splinters that are visible during debridement are removed; no attempt however is made to remove deep, in-driven splinters may necessitate unacceptable brain dissection and retraction and this is likely to aggravate the neurological deficit. 

Careful attention to the missile track and bone and missile fragments is important in minimizing postoperative septic complications. The missile track should be debrided of devitalized and necrotic brain, bone and bullet fragments, the latter if they are readily accessible. The track is gently irrigated with saline or dilute hydrogen peroxide. In wounds that traverse multiple lobes of one hemisphere, the potential for additional iatrogenic injury in following the missile track in its entire length will usually outweigh any potential benefits [18,20,47]. Hemostasis is achieved by conventional techniques, using bipolar coagulator, gentle tamponade with gelatine sponge, oxidized cellulose patties, or even mashed muscle stamps. The cavity should appear clean and hemostasis should be complete. While use of gelfoam or oxidized cellulose can be made to secure hemostasis, they may have to be left in place to control deep seated, obscure bleeding. 

Wounds extending across or abutting the midline pose special problems and injury to the superior sagittal sinus should be presumed to have occurred until proved otherwise. The bone fragment overlying the sinus is gently elevated and sinus bleed is tackled using tamponade. Repair of the sinus may have to be done in case the mid- or posterior third of the sinus is involved. Sinus is repaired using adjacent dura or a patch of vein sutured with continuous 5/0 vicryl suture. 

An exit wound, if present, warrants a local craniectomy, debridement and duroplasty in the same way as described above.

Closure: Dural and scalp closure is axiomatic in the management of CMI. Dural grafts vascularise fast and can be obtained from temporalis fascia, pericranium, fascia lata and transversalis fascia. Galea is required for scalp closure and should not be used as a dural substitute. Artificial dural substitutes with the exception of lyophilized human dura are contraindicated [24]. Scalp flaps can be rotated if required to obtain tension free closure, and closure should be in two layers. Closure of dura and scalp should be meticulous and water-tight. A subgaleal vacuum suction drain can be used once the dura is closed water-tight.

Controversies

Removal of intracranial fragments: Surgical approach described above will result in retention of bone and missile fragments in fair number of patients. Intracranial suppurative sequelae have been a major preoccupation of military neurosurgeons [29,30,43,45]. Martin & Campbell [40] recorded an infection rate of 16% based on their World War II experience; they believed that infections were 10 times more likely than in their absence. In the past, many neurosurgeons dealing with military wounds believed that it was imperative to remove all bone and missile fragments. In fact, reoperation was advocated if retained foreign bodies were demonstrated in the postoperative radiograph [16,29]. However, neurological morbidity of secondary and “second look” procedures is high with enhancement of cerebral oedema and no appreciable reduction in risk of infection [16,17]. It is now believed that retained fragments per se do not increase the risk to infection; in fact there are a number of other factors viz., orbitocranial trajectory, penetration of paranasal sinuses, postoperative CSF leak and persistent elevation of ICP in the postoperative period that are predisposing factors to intracranial suppuration.1 Vrankovic et al reported an incidence of retained fragments in 76.8 % of their cases, with an infection rate of 10 % [57].

With advocacy of less aggressive approach and conservative debridement, there will be higher incidence of retained fragments, especially when the injury is due to splinters from an exploding device. Such injuries are more likely in military personnel, than in civilians, who are more likely to be injured from fire-arm bullets. It has to be understood that the suppurative seuelae are more likely, in case of faciocranial trajectory, skull base involvement, persistent external CSF leak, and elevation of intracranial pressure in the postoperative period [8].

Extent of debridement: Radical debridement of the missile track was practiced by Cushing during the first World War [23]. During early phase of Second World War, during the Korean War, and during the Vietnam War, radical excision was practiced [5,16,39,53]. It was advocated that 0.5 to 1 cm of healthy brain tissue around the missile track be removed [15]. This practice resulted in marked reduction in intracranial suppurative complications. On long term follow up of 1221 patients in Vietnam Head Injury Study in Phase I revealed only 37 cases of brain abscess, of which only 11 were associated with retained bone fragments and all had one or more of other risk factors, viz., postoperative CSF leak, raised ICP in the postoperative period, breach of paranasal sinuses, etc. [16] During Phase II of VHIS, 481 patients were evaluated with CT scan. Retained bone fragments were found in 23 % and all those were free from infection [43].

A more conservative approach has been advocated in recent reports [11,20,27,47]. Brandvold et al [11] reported their experiences in Israeli soldiers injured in the conflict in Lebanon between 1982 and 1985. The policy was to take a less aggressive approach to intracranial debridement with emphasis on the preservation of cerebral tissue, with a conscious effort not to search for in-driven fragments not presenting themselves during gentle irrigation or hemostatic maneuvers. Of 113 patients in their series managed in this fashion, there were 83 survivors, CT scans were obtained in 43, of whom 26 (60 %) had retained metal or bone fragments (or both). None of these patients had suppurative complication(s). Aarabi [2] during Iran-Iraq war practiced gross removal of devitalized brain tissue and of foreign material till normal looking grey and white matter was seen. Vrankovic et al [52] treated CMIs during the Croatian conflict with gentle irrigation and removed bone fragments that presented during this maneuver. There was no increased operative mortality or intracranial sepsis during these series. Similar method of conservative debridement has been practiced in the Indian studies [6,47]. Taha et al advocated simple debridement and closure of the external wound in patients with GCS 10 or above, no exit wound, sparing of the Sylvian fissure region or midline by the missile trajectory, and presenting within 6 hours of injury. [55] They reported only no deaths and only one instance of brain abscess.

Craniectomy or Craniotomy? Harvey Cushing [21] advocated en bloc excision of scalp and bone in the management of CMI. This approach was changed by Matson [41] who advocated centrifugal craniectomy during the Second World war being more expeditious. Ashcroft [5] did not discard the vascularised bone fragments with no apparent septic complications. Sir Hugh Cairns [14] used osteoplastic craniotomy during the World War II. While craniectomy may be more practical in the presence of gross communition and shattered vault, craniotomy too can be carried out in many patients with CMI. In the present of small puncture wounds with little or no contamination, a formal craniotomy can be planned. Even in the presence of multiple fragments, these can be washed with antibiotic solution and replaced after duroplasty; Prakash Singh [47] reported no instance of osteomyelitis with this practice. Unless highly contaminated, cleansed bone fragments should be replaced. 

Timing of Cranioplasty: Based on their results from 417 cranioplasties performed over 13 years while observing a strict protocol of cranioplasty after one year of initial injury, Hammon and Kempe reported excellent results [30]. In another study by Rish et al, infective complications after cranioplasty were seen more often patients who had infection or CSF leak during initial care [51]. There appears to be a general consensus for a period of one year to elapse before cranioplasty can be done in patients with CMI.

Certain Special 

Considerations

Migrating missiles: Retained intracranial metallic fragments may alter their position over a period of time. These fragments may be intraventricular, intraparenchymal or subarachnoid in position. When intraventricular in location, these fragments may shift their position because of availability of space around them, and have been inmplicated in the pathogenesis of hydrocephalus, ventriculitis, hypothalamic dysfunction, etc. [22,49]. A free fragment lying in lateral ventricle can be maneuvered into the occipital horn, from where it can be removed under by ventriculoscopy or stereotaxy [39]. Migration is less often seen in intraparenchymal fragments, since they are surrounded by tissue or gliosis. Migration can occur soon after the injury along the corridors of tissue damage created by tumbling or yawing passage of bullet through the brain. Movements are aided by bullet weight (heavier bullets tend to shift their position), gravity and brain pulsations and sink effect of the ventricles of the brain [42,49]. Delayed migration indicates softening of the surrounding brain, while arrest of migration can occur due to edema, gliosis and due to the fragment getting embedded in a developing brain abscess. Subarachnoid migration can occur through CSF pathways; Young et al [60] reported the spontaneous migration of an intracranial bullet into the cervical canal. 

A migrating missile can result in worsening of neurological deficit due to passage of the bullet through the eloquent brain. Removal can be affected by CT guidance or in case of fragments lying on the cortex, by taking skull radiographs in the operation theatre to localize them precisely immediately prior to craniotomy. Care should be taken to minimize dissection or retraction of brain tissue so as to avoid worsening of neurological deficit. 

Facio-orbito-cranial injuries: Inju­ries sustained by shrapnel from bursting shells, grenades and improvised explosive devices (IEDs) often lead to injuries of face, eyes, neck and chest and upper limbs. Missile wounds that traverse the face prior to entering the intracranial compartment are common. Less common are those missiles which enter the cranium and exit through the face or submandibular region. While the eyeball is usually irreversibly damaged, there may be injury to optic nerve or cavernous sinus and internal carotid artery. In facio-cranial injuries, there is defect in basal dura and communication of subarachnoid space or ventricles with contaminated air-filled spaces with high risk of meningitis and ventriculitis [21,25]. Moreover, defects in basal dura may lead to formation of CSF fistulas. 

In managing these injuries, brain wound takes precedence over facial injuries provided hemostasis has been secured from facial wounds. A uni- or bifrontal bone flap that is large enough to permit visualization of the anterior skull base till the sphenoid wing is made and intradural exploration is done. Damaged brain is debrided and hemostasis is achieved. Optic nerves and chiasma are inspected and dura closed after hemostasis. Dura is separated from the floor of anterior cranial fossa. Bone fragments are debrided and bleeding margins waxed. Ethmoid sinuses are sealed with wax, adipose tissue or mashed muscle. Dura is closed primarily if possible; else, closure is affected with pericranium, temporalis fascia or fascia lata. Mucosa of frontal sinuses is rolled towards their ostia or excised, followed by their exteriorization. 

Neural damage in injuries of the anterior skull base is generally not severe barring the damage to the eyeball or the optic nerve and the since basifrontal region is non-eloquent, and we have not seen any instance of hypothalamopituitary dysfunction in these cases. Hence anterior skull base missile injuries tend to have good prognosis if the initial GCS was high and infection is avoided by early surgery and meticulous dural reconstitution or dural closure [7].

Vascular injuries: Nearly 10 % of military CMIs have dural sinus injury [31]. Hemorrhage from injured dural venous sinuses can lead to rapid exanguination and missiles traversing the midline are associated with poor outcome due to accompanying vascular injury. In survivors who reach medical attention, rent in the sinus is sealed by hematoma or bone fragments, and hemorrhage occurs at the time of debridement. When the location of bone fragments or the path of the missile suggests the possibility of sinus injury, the surgeon must have a clear idea of his operative strategy prior to debridement, and should be mentally prepared to tackle sinus bleed and carry out its repair. Wide bone exposure must be obtained on all sides and the fragment over the torn sinus is removed last. Small tear can be controlled with digital pressure followed by gelfoam soaked in thrombin, or beaten piece of muscle sewn over the rent. With larger rents, this technique may not be adequate. If anterior third of the sagittal sinus is involved, ligation is the procedure of choice. In middle and posterior third, repair of the sinus should be undertaken.

Gunshot injuries to the intracranial arteries can result in occlusion, transection with massive hemorrhage, or traumatic aneurysms. About 80 % of patients with aneurysms have intracerebral hematomas [28]. All patients with injuries in the vicinity of the cavernous sinus, circle of Willis or Sylvian fissure should be evaluated by cerebral arteriography [1]. 

Surgery for Sequelae

CMI patients on follow up over weeks, months or years may have sequelae of the primary injury, or due to retained intracranial fragments which may require surgical intervention. These sequelae are:

CSF Rhinorrhoea: CSF rhinorrhoea due to anterior skull base injury may become apparent in the first few weeks of injury, although it may be seen after several months. There may have be transient cessation of rhinorrhoea in the acute stage due to plugging of the defect by edematous brain. The defect may be in the frontal sinus, cribriform plate or the sphenoid sinus. These patients are investigated by CT cisternography or (in the absence of a retained intracranial ferromagnetic missile) MRI, which shows the site of leakage. Management is by defining the site of leakage by bifrontal craniotomy, and repairing the basal dura with pericranium or fascia lata, followed by plugging the bone defect with bone, bone wax or mashed muscle, with good results. Midline skull base leaks are often amenable to endoscopic repairs.

Brain abscess: Brain abscess is seen in CMI involving the paranasal sinuses, faciocranial trajectory, persistent postoperative CSF leak, intraventricular lodgement of the splinter, etc. [3,8]. Retained intracranial splinters per se are not a significant factor, provided the patient has undergone satisfactory debridement [43]. Brain abscess usually develops within four to six weeks, although they can occur years after the original injury [58]. While serial postoperative CT may diagnose brain abscess in early stages and appropriate antibiotic therapy can be instituted, established abscesses will require excision; the retained splinter is often found embedded in the abscess wall.

Hydrocephalus: The development of hydrocephalus developing after CMI may be responsible for neurological plateauing or deterioration. Hydrocephalus may develop acutely due to subarachnoid hemorrhage. Recurrent bouts of meningitis following CMI may lead to obstructive or communicating hydrocephalus. Hydrocephalus may also occur after excision of brain abscess which was secondary to retained intracranial splinter [9,10]. Pathogenesis of chronic hydrocephalus after head injury is uncertain; subarachnoid spaces in patients dying after head injury and hydrocephalus are obliterated with fibrosis, and ependymal destruction and presence of subependymal gliosis together with loss of white matter especially around the ventricles are prominent findings.61 Experimental studies have shown that there is an increase in the outflow resistance and CSF pressure in rats following subarachnoid infusion of plasma or whole blood and this is due to decrease in transport of fluid across the epithelium of arachnoid villi [12]. All patients who show neurological plateauing after initial improvement, or deterioration, or even those who fail to improve should be investigated with CT to detect hydrocephalus. There is distinct improvement in mental status and cognitive functions of these patients after CSF diversion by ventriculoperitoneal shunting [9,10]. Rarely, hydrocephalus may occur due to occlusion of cerebral aqueduct by a migrating retined missile splinter [44,49].

Prognostic factors

Probably the youngest survivor of CMI has been a 32-week-foetus in-utero [26]. The little one survived not only the bullet wound, but also the subsequent preterm delivery, neonatal intensive care and later removal of the bullet from the brain without any untoward sequel. Prognostic factors are to be considered as they relate to survival and morbidity. Thus, a patient with poor GCS may survive but may be left with devastating neurological deficits or persistent vegetative state. Two factors that have an independent bearing on the survival as well as morbidity are the kinetic energy contained in the missile and the GCS on admission. On the other hand, a high velocity missile generally produces extensive parenchymal damage, and the patient is in a low GCS on arrival; thus GCS is dependent on the amount of energy transfer to the brain by the missile.

Glasgow Coma Scale: The post-resuscitation GCS remains the strongest and most significant predictor of outcome in CMIs. The results of various studies have demonstrated poor outcomes in patients with GCS of 3, 4 or 5 [27,36,37,44]. Postoperative survival rate was 90 % in patients presenting with GCS score of 8 to 14, while all those with GCS 15 survived. [53,54]. Although operative intervention is not of clear benefit to patients with GCS scores of 6 to 8, there are salvageable cases with GCS score of 6 to 8 than with GCS scores of 3 to 5 [33,34,36,37]. It is reasonable to make an effort to identify salvageable cases in patients with GCS scores of 3 to 8, it is likely that surgical efforts may have an impact only on those with admission GCS of 6 to 8. In the war zone, casualties more often suffer from polytrauma as compared with civilian injuries and closed head injuries; war head injury score (WHIS), that incoroporates both GCS and injury severity score (ISS) is an accurate predictor of outcome in the presence of multisystem trauma and CMI [56].

Subarachnoid haemorrhage: Predictive value of SAH in outcome for victims of CMIs has been studied [33,35]. In a study of 100 patients who had sustained CMIs, 68 % of those who died after 48 hours of admission had SAH [37]. Although multiple variables have been associated with poor outcome, presence of SAH is correlated with poor outcome even in the absence of these other variables [36]. 

Vasospasm: Cerebral arterial spasm may occur in CMIs. The association of SAH with CMIs has been investigated by transcranial Doppler to measure blood velocity in middle cerebral artery and in the extracranial internal carotid artery in a series of 33 patients [35]. The frequency of vasospasm was high after CMI (42.4 %) than after closed head trauma (27 %) or after aneurismal SAH (36 %) [34,59]. In all 14 patients suffering vasospasm had CT evidence of SAH, and admission GCS was not a good predictor of vasospasm. Fifty six percent of patients without vasospasm had a favourable outcome, while only 36 % with vasospasm had a favourable outcome (GOS score of 4 or 5).

Pupillary reaction: Pupillary function is a strong predictor of outcome. Only 21 % of those with bilaterally dilated and fixed pupils survive, while 50 % of those with unilateral papillary dilatation survive and survival is 95 % or more in those with bilaterally reacting and equal pupils [46,53].

Coagulopathy: Coagulopathy is a significant predictor of outcome at lower levels of GCS score. An abnormal activated thromboplastin time or prothrombin time on Day 1 was associated with only 20 % survival rate [43]. Kaufman et al have reported that the incidence of a coagulation abnormality was higher in non-survivors as compared to survivors; presence of disseminated intravascular coagulation has an associated mortality rate of 85 %. [32,33]. Shaffrey et al [53] reported on the coagulation profiles in 43 of 62 patients with civilian gunshot wounds. Overall mortality was 55 % and mortality among patients with coagulopathy was 80 %.

Extent of cerebral parenchymal involvement: Significant correlations have been reported between ventricular penetration ande death; 90 % had poor outcome [18] and as many as 84 % cases were fatal in ventricular injury [43]. Nagib et al [44] reported good outcome only in one out of 15 patients with ventricular injury. Bihemispheric involvement has also been found to be predictive of poor outcome [19,32,44].

Hypotension: A systolic blood pressure of less than 90 mm Hg is significantly related to poorer outcome [4,31,33]. This probably is related to poor cerebral blood flow especially in the presence of an intracranial mass lesion. Resuscitation with attainment of normal ICP is associated with survival, while post-resuscitation intracranial hypertension is associated with poor outcome [13].

Conclusion

Operative neurosurgical management of CMI needs a separate orientation from routine neurosurgical procedures. Often the surgery may have to be done under less than ideal conditions, with resources that are barely sufficient, and the biological clock ticking away. A clear understanding of the aim and scope of surgical intervention is essential, so that unrealistic goals are not set or pursued. Debridement with evacuation of hematoma and devitalized brain matter, hemostasis followed by meticulous, tension free dural and scalp closure are the sine qua non of surgical intervention in CMI. The overall results are influenced by a number of factors, the KE in the missile and the initial GCS being the important ones. 

Summary

Craniocerebral missile injuries are a cause of serious concern to a military surgeon operating in battlefield conditions, as well as to his/her civilian counterpart in urban areas or rural hinterland. Successive wars all over the world have witnessed increasing lethality of the missiles, whether bullets or shrapnel, due to their increased accuracy, and higher velocity. Outcome in low velocity missile injuries, as well in those injuries with good Glasgow Coma score has been uniformly good. Injuries due to high velocity impacts on the other hand carry grave prognosis in spite of improved care at the forward echelons, better evacuation facilities and availability of neuroimaging. Neuroimaging and critical care facilities have brought a change in the approach to these injuries. Patients with these injuries can now be selected and operated upon with precision and with a brain-conserving attitude. A less aggressive approach (in comparison to what was being advocated till the seventies) is now a universally followed principle. Predictably, this has led to controversies about the exposure (craniotomy or craniectomy), extent of debridement, attitude towards retained intracranial fragments, and surgery of sequelae, like hydrocephalus, cerebrospinal fluid rhinorrhea, cerebral abscess, etc. Role of critical care and medical management (anti­biotics, cerebral decongestants, anticonvulsants, etc) assumes equal importance with operative management. Patients with retained intracranial splinters need long-term follow-up to detect migration, suppurative complications, hydrocephalus, etc. 

References: ref@mci-forum.com

Author

BG Harjinder S Bhatoe VSM 

BG I/C Adm, Command Hospital (Western Command), Chandimandir, Panchkula, 

Haryana 134107. India

BG H S Bhatoe is a graduate of the Armed Forces Medical College, Pune and was commissioned into the Army Medical Corps in Mar 1979. He has served in a number of medical setups in the peacetime as well as field units, including the elite Parachute Brigade. He was selected to serve with the President’s Bodyguards from 1983 to 1987. He underwent neurosurgery residency at the Postgraduate Institute of Medical Education and Research, Chandigarh (India) in 1990–91. He has published 30 papers in International and more than 85 papers in National journals, and has authored a book on Craniospinal Missile Injuries. At present he is serving in the Command Hospital (Western Command), Chandimandir (Haryana), India. He is a recipient of the Chief of Army Staff Commendation twice – for services rendered in the Northern Command in 1995–1998, and again in Central Command in 1999–2002, and was awarded Vishisht Seva Medal in 2009. He was elected Member of New York Academy of Sciences in 1996, and has been an International Member of Congress of Neurological Surgeons in 2003. 

Address of the author:
BG Harjinder S Bhatoe VSM
Department of Neurosurgery,
Command Hospital (SC)
Pune 411040. Maharashtra. India
Tel: 91-20-26026112
26026412, 26334509
Fax: 91-20-26363302 E-mail: hsbhatoe@gmail.com

Date: 07/05/2012

Source: MCIF 2/12