Case Presentation
A 36-year-old man with penetrating injury to the head due to fishing accident was
referred to Dr. Soetomo General Hospital, a tertiary trauma center in East Java, 10 hours
after the incident. The patient received initial treatment 8 hours after the incident
in a periphery hospital. Due to the assumption of vascular injury, the patient was
referred from the periphery hospital, which is about 65 km from Dr. Soetomo General
Hospital for advance treatment in neurosurgical field. The patient's transportation
took an additional 2 hours. The patient was free from seizure activity as well as
any other sign or symptom of nausea and vomiting. The patient presented with stable
vital signs upon admission, including a total GCS of 15, E4V5M6. The patient showed
no neurological deficits. The only significant symptoms were headache and a history
of bloody rhinorrhea. The patient was transferred to the high-care unit for further
observation and management.
Radiological investigations revealed critical findings. [Fig. 1] shows skull X-ray, which was performed before the patient was transferred to Dr.
Soetomo General Hospital, a foreign object is seen originating from the left nasal
cavity. A computed tomography (CT) scan without contrast revealed no soft tissue edema,
midline shift, or other significant lesions in the epidural, subdural, subarachnoid,
or brain parenchyma spaces as shown in [Fig. 2]. However, a hyperdense lesion in the posterior horn of the lateral ventricle indicated
IVH. The CT scan also visualized a foreign body penetrating from the left nasal cavity,
passing through the ethmoid bone and cribriform plate, with its tip lodged in the
left inferior thalamus.
Fig. 1 Skull X-ray with Caldwell view (A) and Schaedel view (B) consecutively.
Fig. 2 Brain window of noncontrast computed tomography (CT) scan sequentially, coronal view
(A), axial view (B), and sagittal view (C), showing a hyperdense foreign object in the intracranial with intraventricular hemorrhage
(IVH).
[Fig. 3] illustrates CT angiography (CTA) with three-dimensional reconstruction identified
a fracture of the frontal bone with splintering and depression of the inner dome of
the calvarium. The study confirmed the hyperdense lesion in the lateral ventricle,
consistent with IVH, and traced the foreign body penetrating through the ethmoid and
cribriform regions into the left inferior thalamus. The intracranial vessels, including
the anterior cerebral arteries (ACAs), anterior communicating artery, and middle cerebral
arteries (MCAs), appeared normal except for the absence of the left cavernous segment
of the internal carotid artery (ICA).
Fig. 3 Computed tomography (CT) angiography and three-dimensional (3D) reconstruction.
With a transfemoral catheter angiography (TFCA) no evidence of foreign object in the
right ICA was found, and a complete occlusion as high as the petrous segment of the
left ICA was present, as shown in [Fig. 4]. The foreign object was situated at the origin of the ACA and MCA bifurcation, near
the left ICA, suggesting proximity to key vascular structures. The patient then underwent
elective craniotomy with bicoronal incision, clipping of the ICA to prevent excessive
bleeding, as well as backup of endovascular unit, followed with the extraction of
the foreign object on the third day of care as shown in [Fig. 5]. Due to the delay of surgery, controlling intraoperative bleeding presented a significant
challenge, possibly from the collateral artery. Despite these obstacles, through meticulous
technique, teamwork, and the application of hemostatic measures, the bleeding was
ultimately brought under control.
Fig. 4 Transfemoral cerebral angiography (TFCA) of the left internal carotid artery (ICA).
Fig. 5 Intraoperative findings and surgical approach to extract the foreign object. (A) Preservation of the olfactory nerve, (B) followed by clipping of the internal carotid artery (ICA) to prevent bleeding and
cautious extraction of the foreign body. (C) An example of the foreign object.
Postoperatively, on the fourth day, the patient was intubated with sedation and intensive
monitoring in the ICU. In the ICU, the patient's fluid balance was meticulously managed
through the administration of intravenous crystalloids. To prevent raised intracranial
pressure (ICP) and associated complications, metamizole was administered for analgesia,
omeprazole for gastric ulcer prophylaxis, and metoclopramide to prevent nausea and
vomiting. Antiseizure prophylaxis was provided using phenytoin, and broad-spectrum
ceftriaxone was prescribed for infection prevention. Additionally, a precautionary
dose of tetanus vaccine was administered due to the high risk of tetanus associated
with the presence of a foreign body. From postoperative laboratory evaluation, the
patient hemoglobin was low[8]
[9] due to excessive intraoperative bleeding, hence transfusion of two units of whole
blood was done.
On the eighth day of the patient's ICU stay, a thorough physical examination was conducted
to assess his condition. During this evaluation, it became evident that the patient
exhibited inadequate responses, indicating significant neurological impairment. Subsequently,
further clinical assessment led to the diagnosis of brain death. Despite efforts to
monitor and support the patient, his condition worsened, and eventually entered an
apnea state. Given the absence of any respiratory effort, the patient was pronounced
dead shortly thereafter.
Discussion
Effective transport and EMS have significant role to improve prehospital time and
improve patient outcomes in life-threatening trauma in low- and middle-income countries
(LMICs). Inefficiencies in EMS, such as poor referral systems and long distances,
are among the main reasons why patients take too long to seek help in certain conditions
such as nonmissile penetrating head trauma, which often require surgical intervention
within 12 hours to reduce morbidity and mortality.[18]
[19]
The method of transportation and the efficiency of EMS play a crucial role in reducing
prehospital delays and improving patient outcomes, especially in LMICs. The poor efficiency
of EMS is shown with the arrival time at tertiary trauma centers, which took more
than 8 hours, in correlation to the study by Karthigeyan et al,[20] where only 17.8% trauma patients reach tertiary trauma centers within 6 hours of
injury.[20] Indirect patient transport has been associated with an increased risk of short-term
mortality. Although a statistically significant relationship has not been established
from recent studies, mortality rates consistently remain elevated during interhospital
transfer processes. Therefore, in trauma cases, it is strongly recommended to prioritize
direct transfer to appropriately equipped medical facilities whenever feasible, as
this approach has the potential to improve patient outcomes and reduce mortality risks.[21]
Studies show that significant number of patients rely on private transportation, such
as personal vehicles, for emergency hospital visits, leading to considerable delays.
For instance, in East Java, Indonesia, 67.25% of patients with neurological emergency
used private transportation, resulting in delays ranging from 2.4 to 48.4 hours, while
only 32.75% used ambulances with approximate transfer distance ranging from 3.5 to
18.4 km.[22] Our case highlights a longer travel distance required by the patient, since the
trauma site is located in rural area, than the findings from Ningsih and Andarini,[22] due to the lack of tertiary trauma center in East Java Province. The primary destination
for advanced trauma care, Dr. Soetomo General Hospital, is located approximately 80 km
from the trauma site, hence creating arrival delay exceeding the golden hour, allowing
secondary brain injury sequelae to progress as well as decreasing the patient's outcome.
Contrary to urban settings, rural regions have demonstrated a far greater mortality
risk for trauma cases. Rural trauma patients are at a two times greater risk of mortality
because they have to endure the durability of the transportation and the increased
distance to the trauma care centers as research shows.[23]
[24]
[25] Moreover, a study conducted by Caviglia et al[26] highlight that every additional minute of delay, whether during prehospital care
or within the hospital, is associated with a corresponding increase in both mortality
and morbidity.[26]
Alternative transportation methods, such as modified motorcycle called as motor-lances
and helicopters, have been shown to reduce response times and improve patient outcomes,[27] although another study by Cunningham et al[28] suggest that the survival benefits of helicopter transport may only apply to a limited
subset of patients.
These delays are further compounded in LMICs due to fragmented EMS systems, inadequate
infrastructure, and a shortage of trained personnel and basic life support tools.
The standard of medical services offered to citizens by the EMS providers has to be
guaranteed, as one study in Cambodia and Iraq showed a 30% decreased mortality as
the EMS providers were trained to provide onsite management.[29] To address these challenges, improvement of EMS provider quality, investments in
structured prehospital care systems, wider adoption of advanced transportation methods,
and improved access to ambulances equipped with trained personnel are essential. Such
measures can significantly reduce prehospital delays and enhance patient outcomes
in resource-constrained settings.
In Indonesia, this problem is exacerbated by the lack of health facilities and specialists.
Studies indicate that proximity to trauma centers is directly associated with improved
survival rates following traumatic injuries. Brown et al[30] highlighted that rural populations face significant barriers to accessing trauma
care, resulting in higher injury-related mortality compared to urban areas. Moreover,
a study by Daugherty et al[31] underlined that more than 80% rural residents were hospitalized in urban hospital,
which may contribute to the higher rate of TBI-related deaths in rural areas, indicating
a lack of emergency care services in those regions.
The ratio of neurosurgeons to population is still twice the ratio proposed by the
Indonesian Neurosurgery Association, meaning complex cases need longer time to be
referred to better facilities for definitive care as well as indicating discrepancy
of trauma care in rural and urban area.[32] Another major concern worth discussing is the distributions of neurosurgeons in
Indonesia since 5 out of 34 provinces are not covered by neurosurgery specialist as
of 2020. Based on the data by the Indonesian Health Ministry, Southeast Asia has the
lowest number and distribution of neurosurgeons compared to other parts of the world.
This imbalance is due to the lower number of surgeons trained in the discipline of
neurosurgery, leading to poor coverage and underserved health services for the population.
[32]
[33] Regional distribution and resource shortages lead to an estimated 2.5 million unaddressed
primary neurosurgical operations each year in Southeast Asia.[33]
[34]
[35] Additional time needed to reach facilities with neurosurgeon takes time, hence delaying
patients to get immediate intervention. Addressing these systemic challenges requires
substantial investments in EMS infrastructure, equitable distribution of specialists,
and improved referral systems to ensure timely and efficient access to specialized
care, ultimately reducing delays and improving outcomes for trauma patients in Indonesia.
The study provides insights into how health care systems influence delays in managing
TBIs, which correlated with the National Insurance System, referred to as BPJS (Badan Penyelenggara Jaminan Sosial) in Indonesia, which uses a single-payer health system (SPHS). A study by Shakir
et al,[19] compare the prehospital and intrahospital delays of SPHS and multi-payer health
system (MPHS) where the SPHS exhibits shorter prehospital delays compared to the MPHS
but has prolonged intrahospital delays.
In our daily practice, the National Insurance System has been linked to longer interhospital
delays in Indonesia. This paradox may arise due to specific implementation challenges
of the National Insurance System in resource-limited settings, such as the bureaucratic
processes for claim approvals, lack of adequate emergency transport infrastructure,
and delays caused by administrative checks before patient transfer. In comparison,
the SPHS framework in other countries highlights that centralized coordination and
equitable access can reduce prehospital delays. In Indonesia, these theoretical advantages
are overshadowed by systemic inefficiencies in execution. Furthermore, as seen in
SPHS globally, intrahospital delays under the National Insurance System could also
be prolonged due to resource limitations and patient volume, mirroring the longer
intrahospital delay (mean = 309.37 minutes, confidence interval [CI] = −21.95 to 640.69),
which also contributed to the patient's arrival time delay at the tertiary trauma
center.[19]
The verification process for the National Insurance System health claims is significantly
slow, creating inefficiencies that deviate from the guidelines of the National Insurance
System Health Regulation Number 3 of 2017, which mandates a maximum of 15 working
days for claim processing. In practice, hospitals face challenges in meeting this
timeline, especially when dealing with traumatized patients who often struggle to
categorize their cases under the category of Health or Employment insurance in the
National Insurance System, as observed in the Taluk Kuantan Regional Hospital.[36] This issue aligns with the findings from Allahabadi et al,[37] who noted that public or government insurance contributes to substantial treatment
delays. Their study revealed that adult patients with public insurance experience
approximately 6 times longer wait times for clinical evaluation, 5.5 times longer
for radiological scans, and 4.5 times longer for surgery compared to those with private
insurance. Such delays negatively affect patient care, prolonging access to critical
medical procedures and increasing the risk of complications. These inefficiencies
in the National Insurance System highlight the broader challenges faced by public
insurance schemes and emphasize the urgent need for reforms to streamline claim verification
processes, ensuring timely medical interventions and reducing disparities between
public and private health care services.[37] Financial barriers further exacerbate the situation, preventing many patients in
LMICs from affording critical investigations and essential surgical procedures.[38]
Delays in diagnostic imaging also pose significant challenges, with median waiting
times for CT scans in LMICs ranging from 37 minutes to 7 hours, creating detrimental
variations for patient care.[38] CT scan is the most readily available and reliable radiological modality for patients
with PBIs, offering rapid and detailed evaluation of both bony structures and soft
tissues.[39] These findings are linear with our case findings, where the patient needed to travel
for 80 km to acquire CT scan as the primary radiological modality in TBI.
CT scan is usually performed in emergency situations due to its time efficiency and
provides detailed findings on brain structures. CT scan is essential for the diagnosis
of acute as well as chronic intracranial lesion, such as intracranial hemorrhagic
lesion and infarct.[1]
[40] The usage of CT scan in PBI cases is not only to visualize the injury that caused
it but also to evaluate the associated soft tissue as well as vascular damage. In
cases where a penetrating vascular injury following PBI is suspected, CTA is highly
recommended to assess the vascular architecture and rule out any vascular injury such
as pseudoaneurysm or vascular occlusion.[41]
[42]
[43] Another radiological modality, digital subtraction angiography (DSA) is considered
the gold standard for diagnosing vascular lesions due to its superior accuracy compared
to CTA, highlighting DSA's higher sensitivity, specificity, positive predictive value,
and negative predictive value, emphasizing the need for DSA when vascular injury is
suspected.[44]
However, requirement to advanced diagnostic facilities, such as CT scan, CTA, and
DSA, is often not met promptly in LMICs, including in East Java province. A study
by Zimmerman et al[45] recorded one-fourth of TBI patients do not receive adequate radiological imaging
in the emergency unit, although there is indications for radiological imaging in LMICs.
This is vital, since vascular injury complicate the treatment and strategy to manage
PBI, and the involvement of vascular injury requires rapid intervention as well as
resulting in different strategy for surgical intervention.[46] These studies align with our case presentation, where a difficulty to obtain adequate
radiological imaging is present in the periphery hospital emergency room, hence raising
the risk of mortality and morbidity by delaying diagnosis and detection of related
complications. In the end, due to this burden, the neurosurgery team faces vivid difficulties
in implementing the right strategy for handling head trauma cases, especially PBI
in Indonesia.
Seelig et al[47] found that patients who underwent surgery within the first 4 hours had a significantly
lower mortality rate of 30%, compared to a staggering 90% for those treated after
4 hours (p < 0.0001). Similarly, research by Okada et al[48] analyzed 1,169 trauma patients who received definitive care within 4 hours and survived
beyond that period. Of these, 33% (386 patients) ultimately died, with the median
time to care being 137 minutes. However, only 5.2% (61 patients) were treated within
60 minutes of injury. Due to multifactorial limitations as explained above, the foreign
object extraction could only be done approximately 72 hours postinjury, hence, we
highlight this phenomenon as one of the contributing factors related to the patients'
mortality.
Following TBI, patients often experience global and localized changes in cerebral
blood flow (CBF). During the first 12 hours postinjury, reduced perfusion is typically
observed, followed by hyperperfusion and potential vasospasms, which may eventually
normalize. Hyperperfusion can lead to premature capillary structures that are prone
to disruption during surgical interventions, resulting in secondary bleeding.[49]
[50] This may have correlation with the finding of excessive bleeding intraoperatively,
and might be the cause of the patient's deterioration.
In addition, up to 40% of cases of PBI report vascular complications such as secondary
intracranial hemorrhage, pseudoaneurysm, traumatic aneurysms, and vasospasm. Timely
treatment of these complications is critical and recent evidence supports the universal
application of CT scanning and CTA during the 24 hours after the surgical approach
for effective and early surveillance for any complication process.[51]
[52]
[53]
Cerebral vasospasm is a significant complication following subarachnoid hemorrhage
(SAH) and TBI, necessitating routine postoperative imaging for early detection. Radiological
modalities such as CTA and CT perfusion imaging are highly effective in identifying
vascular changes and detecting ischemia associated with vasospasm.[54]
[55] This is particularly critical for TBI patients, where maintaining cerebral perfusion
pressure (CPP) is vital to avoid secondary brain injury.[56] Robust monitoring through transcranial Doppler as well as CT scan facilitates proactive
management strategies, including fluid resuscitation and vasodilator intervention,
that help mitigate the progression of vasospasm to ischemic lesions. Vasospasm, characterized
by the narrowing of cerebral arteries due to smooth muscle contraction and inflammatory
infiltration, significantly diminishes cerebral perfusion and results in the failure
of cerebral autoregulation, microthrombosis, and cerebral ischemic injury.[57]
[58]
Cerebral vasospasm and delayed cerebral ischemia (DCI) are significant complications
following TBI, contributing to increased morbidity and mortality by disrupting CBF
and leading to secondary brain injury. On the third day after the accident, the patient
had undergone TFCA and the total occlusion in the ICA was as high as the petrous level.
Since the arrival time to the tertiary trauma center is prolonged, vasospasm is neglected,
creating total occlusion of the ICA and as a consequence might proceed to cerebral
ischemia.
Posttraumatic vasospasm (PTV) has been closely linked to unfavorable outcomes in TBI
patients, especially with low-velocity PBIs. A study by Almojuela et al[59] found that only 35.7% of patients with vasospasm achieved a favorable Glasgow Outcome
Score, compared to 47.4% of patients without vasospasm, although this difference did
not reach statistical significance (p = 0.12) . Similarly, Prasad et al[60] reported that vasospasm is associated with a 20% incidence of morbidity and mortality
in patients with SAH, underscoring its critical role in the development of secondary
injuries.
Vasospasm significantly reduces neurological outcomes, with less than 20% of head
trauma patients exhibiting clinical deficits experiencing poor prognoses. The reported
incidence of PTV ranges from 19 to 68%, and it is often associated with decreased
likelihood of routine discharge, extended hospital stays, and reduced overall survival
rates.[61]
[62] The pathophysiology of vasospasm includes mechanisms such as reduced nitric oxide
production, direct calcium channel activation, inflammation, and oxidative stress,
which collectively impair cerebral autoregulation and promote microthrombosis and
ischemic injury.[58]
Several factors contribute to PTV, including SAH, low GCS scores, and metabolic factors,
such as hypoalbuminemia, which impairs blood–brain barrier (BBB) integrity and exacerbates
cerebral edema.[63]
[64] Metabolic complications such as anemia and thrombocytopenia further contribute to
cerebral ischemia by reducing oxygen-carrying capacity and inhibiting angiogenic responses.[65]
[66] Hypoalbuminemia exacerbates BBB disruption, leading to vascular leakage, increased
cerebral edema, and secondary hemorrhages, which amplify the risk of ischemia and
infarction.[67] These complications are compounded by logistical challenges, such as delays in diagnostic
imaging, insurance system issue, travel distance, and inadequacy of advance care facilities.[20]
[22]
[38]
[46]
The management of PTV following TBI in the ICU remains ambiguous due to the lack of
definitive guidelines. Research by Ha et al[68] and Francoeur and Mayer[69] emphasizes the importance of monitoring vessel caliber over time using transcranial
Doppler and CTA, particularly during the 3rd to 7th days postinjury, to manage vasospasm.
Early identification of vasospasm allows for timely therapeutic interventions, such
as vasopressor therapy and fluid resuscitation, aimed at optimizing CPP and preventing
further secondary brain injury. A different outcome is found in a similar case reported
by Almojuela et al.[59] The diagnosis of vasospasm took shorter time than ours, resulting in different strategy
implementation mainly to focus on managing PTV with pharmacological therapy and balloon
angioplasty, given its potential reversibility. This study also highlights the importance
of repeat CTA to ensure the resolution of vasospasm as well as the presence of possible
postoperative complications. The patient survived and was discharged from hospital
6 weeks postadmission.
In this patient, we evaluated the IVH as a posttraumatic complication to the PBI,
whereas IVH stands as a risk factor for secondary intracranial arterial lesion, hence
resulted in several vascular complications.[70]
[71] The course of PBI is one of the determinants of patients' outcome. Similar researches
show that PBIs that penetrate through the ventricle significantly increase the chances
of developing secondary IVH and obstructive hydrocephalus in which mortality rates
can be as high as 54%.[12]
[13]
One of the acceptable laboratory and radiology monitoring by the national health insurance
(BPJS) is routine blood test. Routine blood tests are widely used for patient monitoring
in Indonesia due to insurance limitations, and unfortunately, it does not provide
a complete picture of the patient's condition. Before the clinical deterioration,
anemia (8.9) and thrombocytopenia (112,000) were identified, followed by hypoalbuminemia.
While these findings are valuable, they may not capture the nuanced progression of
a patient's clinical condition. This limitation calls for enhanced diagnostic strategies
to monitor patients more comprehensively. Integrating advanced imaging techniques
or frequent neurological assessments could complement routine blood tests and improve
early detection of complications. Expanding monitoring protocols is essential to bridge
the gap in patient care and ensuring timely interventions.
Anemia is a critical systemic factor that exacerbates secondary brain injury in patients
with TBI. Anemia compromises the oxygen-carrying capacity of the blood, leading to
inadequate cerebral oxygenation, which worsens ischemia in brain-injured patients.[72]
[73] Following TBI, the brain enters a hypermetabolic and hypercatabolic state that heightens
the demand for oxygen and nutrients. This state accelerates the depletion of red blood
cells and hemoglobin, further compounding the effects of anemia.[74] A retrospective study on 1,150 TBI patients found that anemia, defined as hemoglobin
levels below 9 g/dL, was significantly associated with increased mortality (odds ratio = 3.67;
95% CI = 1.13–2.24).[65] The hypermetabolic state of the injured brain, combined with anemia, creates a mismatch
between oxygen supply and demand, worsening ischemia and leading to poorer outcomes.
Thrombocytopenia and hypoalbuminemia are critical systemic factors that exacerbate
secondary brain injury in patients with TBI, significantly contributing to poorer
outcomes. Postoperative thrombocytopenia is associated with poor short-term prognosis
in TBI patients, as it inhibits the angiogenic response, leading to brain tissue ischemia.[75]
[76] Moreover, 50% of moderate-to-severe TBI patients with thrombocytopenia develop new
or progressive lesions visible on follow-up cerebral CT scans, highlighting its role
in worsening secondary injuries.[76] Similarly, hypoalbuminemia disrupts the integrity of the BBB, promoting plasma leakage
into the extravascular space and intensifying cerebral edema.[77]
Thrombocytopenia diminishes platelet count, impairing angiogenesis, which is essential
for restoring vascular stability and perfusion to ischemic brain tissue after TBI.
This impairment promotes tissue ischemia, further compounding the severity of secondary
brain damage. On the other hand, hypoalbuminemia exacerbates the breakdown of the
BBB, leading to increased vascular permeability, plasma leakage, and cerebral edema.
This leakage heightens ICP and contributes to secondary brain injury.
The cause of death in this patient is likely multifactorial, with DCI being a significant
contributor. In Indonesia, routine radiological monitoring in the neuro-ICU, such
as CTA or transcranial Doppler, is often limited due to insurance constraints, leaving
patients vulnerable to undetected complications. The ICA occlusion on the third day
after the incident suggests a high likelihood of DCI, as the blockage would severely
impair cerebral perfusion, particularly in regions without sufficient collateral circulation.
The absence of adequate vasospasm treatment, such as nimodipine therapy in the neuro-ICU,
further exacerbates ischemic risk, as unmitigated vasospasm can compromise CBF. Additionally,
the hypermetabolic and hypercatabolic state of the injured brain, combined with systemic
factors like anemia and thrombocytopenia, likely worsened the oxygen supply–demand
mismatch, intensifying ischemic damage and contributing to secondary brain injury.
Another probable cause of death could be rebleeding, particularly given the postoperative
thrombocytopenia and the presence of IVH. Low platelet levels hinder clot stabilization,
raising the risk of vascular rupture, especially in fragile, newly formed vascular
structures. Complication of the foreign object's trajectory, in this case IVH, points
to a hemorrhagic process that could raise ICP, leading to herniation or further compromising
cerebral perfusion. The delayed extraction of the foreign object, occurring past the
golden hour for intervention, also significantly increased the risk of mortality by
allowing ischemic and hemorrhagic processes to advance. The limited monitoring and
therapeutic options available in the ICU setting due to financial and systemic barriers
likely prevented timely identification and management of these complications, resulting
in poor outcomes. Together, DCI, rebleeding, and systemic factors like anemia, thrombocytopenia,
and hypoalbuminemia culminated in a fatal progression of secondary brain injury, hence,
decreasing the patient's survival chance.
This case report offers a comprehensive analysis of the factors influencing mortality
in PBI, with a particular focus on socioeconomic determinants, such as the National
Insurance System. It highlights the challenges faced in accessing tertiary trauma
centers, compounded by inadequate facilities, particularly radiological resources,
in peripheral hospitals. Additionally, the report addresses the limitations of neuromonitoring
in the management of PBI patients, emphasizing its critical role within the context
of the National Insurance System.
This study has several limitations that must be considered. First, the cause of death
in our case remains undetermined due to the limitations in radiological monitoring,
which hindered a more comprehensive assessment of critical conditions. Second, minimal
data regarding the reasons for delayed arrival at trauma centers restricts our understanding
of prehospital factors impacting patient outcomes. Third, there is a paucity of studies
reporting PBI cases with similar outcomes, limiting the generalizability of our findings.
Furthermore, few studies have explored the relationship between insurance systems
and mortality in PBI patients, particularly within the context of Indonesia, an area
that warrants further investigation. Lastly, the interhospital referral system, particularly
its interaction with national health insurance, remains understudied, and its potential
impact on trauma patient outcomes requires more focused research.
This study highlights the need for more research on PBI in Indonesia. Increasing publications
and studies on PBI will improve local understanding and management. It is also crucial
to raise awareness of vascular complications in PBI and encourage research in related
fields such as vascular surgery and trauma care. Future studies should examine how
the National Health Insurance (BPJS) system affects neuromonitoring practices in PBI
cases, aiming to improve health care delivery. Additionally, analyzing factors affecting
patient outcomes—from prehospital care to management and intensive care monitoring—will
help develop recommendations to optimize PBI care in Indonesia.
