Head Trauma or Traumatic Brain Injury

#### **Chapter 6**

## Management of Traumatic Brain Injury

*Soe Wunna Htay*

#### **Abstract**

Head trauma or traumatic brain injury (TBI) is one of the most serious, life-threatening conditions in trauma victims. Prompt and appropriate therapy is essential to obtain a favorable outcome. The aim of the acute care of patients with brain injury is to optimize cerebral perfusion and oxygenation and to avoid secondary brain injury. Secondary brain injury develops with times and cause further damage to nervous tissues. The common denominators of secondary injury are cerebral hypoxia and ischemia. A systemic approach such as the Advanced Trauma Life Support (ATLS) algorithm has been recommended for managing head injury patients. Quick initial assessment of the patient's neurologic condition thoroughly is mandatory. There should be attention in evidence of intrathoracic or intraperitoneal hemorrhage in multiple traumatized patients. Optimizing the open airway and adequate ventilation depending on patient's neurologic condition is first step in emergency therapy. Cerebral perfusion pressure should be maintained between 50 and 70 mmHg. Systemic hypotension is one of the major contributors to poor outcome after head trauma. Careful stabilization of the blood pressure with fluid resuscitation and a continuous infusion of an inotrope or vasopressor may be necessary. Standard monitoring with direct arterial blood pressure monitoring and periodical measurement of arterial blood gases, hematocrit, electrolytes, glucose, and serum osmolarity are important. Brain monitoring as with an electroencephalogram, evoked potentials, jugular venous bulb oxygen saturation (Sjo2), flow velocity measured by transcranial Doppler (TCD), brain tissue oxygenation (btPo2), and ICP monitoring may be used. The reduction of elevated ICP by means of giving barbituates, hyperventilation, diuretics and hyperosmolar fluid therapy, body posture and incremental CSF drainage are critical. Seizure prophylaxis, early enteral feeding, stress ulcer prophylaxis, prevention of hyperglycemic state, fever and prophylaxis against deep venous thrombosis in neurointensive care unit are also important after successful resuscitation of head trauma patients.

**Keywords:** traumatic brain injury, head trauma

#### **1. Introduction**

Head trauma or traumatic brain injury (TBI) is one of the most serious, life-threatening clinical problem related with long-term neurobehavioral and socioeconomic consequences in trauma victim [1].

Prompt and appropriate therapy is necessary to obtain a favorable outcome. The management of patient with head injury focuses aggressively on the

stabilization and resuscitation of the patient from hypoxia, hypoventilation and cardiovascular collapse. These preventable and treatable secondary insults can complicate the course of patients with head injuries and adversely affect outcome.


### **2. Systemic and intracranial causes of secondary brain injury**

The neurosurgical team members especially anesthesiologists manage perioperative course, taking the patients from the emergency room to the neuroradiology suite, the operating room, and the neurointensive care unit.

#### **3. Emergency management**

#### **3.1 Initial assessment of the patient's condition**

Glasgow Coma Scale (GCS) assessment can be used for assessing neurologic condition of head trauma patient. Trained health care providers can measure GCS. GCS is based on 15 point scale for estimating severity of brain injury following trauma [2].

1.GCS score of 3 to 8 represents severe head injury.

2.GCS score of 9 to 12 represents moderate injury.

3.GCS score of 13 to 15 represents mild injury [3].

Pupillary responses (size, light reflex) and symmetry of motor function in the extremities should be quickly examined [4].

Head trauma patients are also associated with injury to other parts of body. If the patients presented with shock, thoracic and abdominal injury should be assessed for intrathoracic or intrabdominal bleeding.

#### **3.2 Advanced trauma life support (ATLS) algorithm**

There is best accomplished by using a systemic approach, Advanced Trauma Life Support (ATLS) algorithm, which consists of primary and secondary surveys of the patient.

#### *3.2.1 Primary survey*

A brief history taking and examination have to be performed within a short period. The history is obtained according to the AMPLE mnemonic (allergies, medications, past medical history, last meal and event). Examination and immediate resuscitation are performed according to the ABCDE mnemonic (airway, breathing, circulation, disability, exposure).

i. Airway management of the patient: The careful monitoring of changes in mean arterial pressure (MAP), intracranial pressure (ICP), and partial pressures of arterial carbon dioxide (PaCO2) and oxygen (PaO2) during airway management of traumatic brain injury patent is essential.

Indications for intubation include


If the cervical spine injury has not been precluded, manual in line stabilization of head and neck is important during endotracheal intubation. Rapid sequence induction and intubation have to perform in patient with full stomach, using direct laryngoscopy. Flexible fiberoptic intubation may be valuable in patient who have difficult airway and unstable cervical spine fractures. Laryngeal mask airways (LMAs) including the intubating LMAs and surgical airway techniques such as cricothyroidotomy and tracheotomy are useful back up techniques for ventilation and intubation.

Intravenous uses of lidocaine, 1.5 mg/kg as a pretreatment before endotracheal intubation has been shown to blunt the increase in ICP in response to airway manipulation [6]. If the vital signs of patient are stable, using propofol and thiopental during induction can decrease intracranial pressure and cerebral metabolic rate of oxygen consumption (CMRO2). While hemodynamic condition of the patient is unstable etomidate 0.3 mg/kg may be a better choice [7].

Use of muscle relaxants facilitate tracheal intubation and decrease the risk of straining. 1 to 1.5 mg/kg of depolarizing muscle relaxant, succinylcholine can be given in emergence condition. Succinylcholine is contraindicated in TBI associated with spinal cord crush, or burn injury owing to the risk of hyperkalemia [8]. Nondepolarizing neuromuscular blocking drugs (NDNMB) including rocuronium, 1 mg/kg, and mivacurium, 0.2 mg/kg, do not increase ICP and can be used in endotracheal intubation in emergence condition. However, nondepolarization muscle relexants use have a slower onset of action (60 to 90 seconds) and caution with allergy using these agents [9].

ii. Breathing considerations include the following: Supplemental high-flow oxygen is provided to all patients to prevent hypoxia (PaO2 <90 mm Hg) regardless of patient's neurologic condition. Positive pressure ventilation is provided to maintain adequate ventilation and oxygenation [10]. In patients who are hypovolemic, PEEP >10 cm H2O may reduce CBF. Continuous infusion of sedative and analgesic drugs is beneficial in mechanical ventilated patients for synchronizing of ventilation strategy [11].


#### *3.2.2 Secondary survey*

Thorough history taking and physical examination, laboratory testing such as metabolic panel, complete blood count, prothrombin time (PT) and partial thromboplastin time (PTT), urinalysis, ethanol level, urine drug screen, and blood type and screen, radiological examination of the whole body should be carried out in secondary survey.

### **4. Monitoring of patients with traumatic brain injury**

#### **4.1 Intracranial pressure (ICP) monitoring**

In clinical practice, invasive and non-invasive methods of ICP monitoring are used aiming to determine the optimal cerebral perfusion pressure (CPP). Monitoring of ICP is useful, not only as a guide to therapy, but also for assessing the response to the therapy and determining the prognosis.

Brain Trauma Foundation Guidelines lists the following indications [14]:

1.Moderate to severe head injury patient with normal CT scan

2.Two or more following features are noted in admission:

Age > 40 years, BP < 90 mmHg and Unilateral or bilateral motor posturing

#### *4.1.1 Invasive ICP monitoring*

Today, the intraventricular catheter remains the gold standard for ICP monitoring, as it measures global ICP [14]. Moreover, the intraparenchymal catheters used for ICP monitoring have integrated as a CSF drainage catheter and catheters that detect parameters, such as brain tissue O2 partial pressure (PbtO2) and cerebral blood flow (CBF).

#### *4.1.2 Non-invasive ICP monitoring*

A non-invasive ICP monitor should be readily available throughout the hospital, be inexpensive, accurate and convenient to use.


#### *4.1.3 Additional tools in ICP monitoring*


#### **4.2 Others standard monitoring**

Baseline monitoring should include electrocardiography, pulse oximetry, capnography and urine output. Invasive hemodynamic monitorings like invasive arterial pressure measurement and central venous pressure is essential in TBI patients [25]. Some of hemodynamic unstable patients need pulmonary artery catheter placement.

Invasive arterial pressure monitoring permits assessment of beat-to-beat variation in blood pressure and regular arterial blood-gas sampling. Central venous pressure monitoring helps optimization of fluid balance and giving vasoactive drugs and parenteral nutrition. Insertion of a pulmonary artery catheter allows the accurate measurement of pulmonary vascular pressure and calculation of cardiac output. Blood glucose, electrolytes, hematocrit, serum osmolarity and coagulation should be monitored periodically [25].

Insertion of an indwelling urinary catheter facilitates measurement of urinary volume and composition of urine. It helps diagnosis of conditions of altered urinary output associated with TBI such as diabetes insipidus (DI), the syndrome of inappropriate antidiuretic hormone (SIADH) secretion, cerebral salt wasting syndrome and the hyperosmolar state [26].

#### **5. General critical measures**

Multiple treatment options exist to treat acute intracranial hypertension. The goal of these therapies is to control ICP to less than 20 mmHg [27] and improving parameters. The most recent TBI guidelines from the Brain Trauma Foundation (BTF) suggest that the ICP goal should be less than 22 mmHg [13].

#### **5.1 Intubation and mechanical ventilation**

Early and rapid intubation and mechanical ventilation have to be practiced in moderate to severe head trauma patients [5]. During intubation, adequate depth of sedation and elimination of reflexes such as cough and vomiting should be achieved. Mechanical ventilation should aim at avoiding hypoxemia, hypercapnia and hypocapnia [5]. The usual PCO2 should be kept at values between 35 and 40 mmHg [27]. Generally positive end expiratory pressure (PEEP) can increase intrathoracic pressure and decrease cerebral venous drainage from superior vena cava [28]. PEEP >15 cmH2O can be applied safely in patients with acute brain injury as it does not have a clinically significant effect on ICP or CPP [10].

#### **5.2 Blood pressure (BP): CPP optimization**

Cerebral perfusion pressure (CPP) is key component in management of traumatic brain injury. Cerebral perfusion pressure is defined as mean arterial pressure (MAP) minus intracranial pressure (i.e., CPP=MAP-ICP) [29]. The recommended goal of CPP per BTF guideline is 50–70 mm Hg [30]. CPP less than normal limit may result in ischemic brain injury [30]. CPP directed therapy is based on theoretical aids that maintaining optimal cerebral blood flow is necessary to meet the metabolic needs of the injured brain [31]. The "Lund therapy" is a therapeutic approach that focuses on the reduction of ICP by decreasing intracranial volumes [32].

Brain trauma foundation guidelines suggest that SBP ≥ 100 mmHg should be maintained for patients 50 to 69 years old or ≥ 110 mmHg for patients 15 to 49 years or > 70 years old to decrease mortality and improve outcomes [13].

Improving outcome of high-risk surgical patients depend on optimizing cardiac output and oxygen delivery guided by goal-directed fluid therapy (GDT) [33]. Crystalloids, colloids and blood components are used for fluid resuscitation and conserving cardiovascular stability to ensure adequate tissue perfusion. Fluid resuscitation should be guided not only by blood pressure but also by urinary output and central venous pressure (CVP) [34]. Hypotension may worse neurologic outcome [35].

0.9% normal saline remains widely used as a resuscitation fluid and remains the fluid of choice for patients with brain injury [36]. Lactated Ringer's solution is slightly hypotonic relative to plasma. Osmolarity should be frequently checked if large amount of lactate ringer solution is used [37]. Hypoosmolar solutions like 5% dextrose in water increase brain water content and consequently increase ICP. Glucose containing solutions are avoided because hyperglycemia is associated with worsened neurologic outcomes [38].

Large volumes (>500 mL) of 6% hetastarch should not be used because they may cause coagulopathy [39]. Patients who have hemoglobin (Hb) (7-8 mg/dl) may require blood and blood products transfusion to optimize oxygen delivery [40]. By reducing oxygen delivery, anemia may aggravate secondary insult of traumatic brain injury [41].

#### *Trauma and Emergency Surgery*

If the blood pressure and cardiac output cannot be restored through fluid resuscitation, continuous administration of inotropic and vasopressor drugs is necessary. An infusion of either phenylephrine or dopamine is recommended to maintain cerebral perfusion pressure (CPP) [13, 15].

#### **5.3 Body positioning**

Elevation of head position 20–30 degree may be helpful in managing ICP [42]. Preventing excessive flexion or rotation of the neck, avoiding restrictive neck taping, and minimizing stimuli that could induce cough and Valsalva responses and uses of lignocaine during endotracheal suctioning are important in management of intracranial hypertension [43].

#### **5.4 Temperature control**

It has been shown that patients who develop a body temperature > 37.5°C within the first 72 hours, have significantly worse outcomes determined as Glasgow outcome scale (GOS) 1 or 2 [5, 16, 44]. These include intravenous and enteral antipyretic medications, control of room temperature, and cooling blankets or pads [16].

Although hypothermia (32 to 34°C) decreases cerebral metabolism and may reduce CBF and ICP [19], therapeutic hypothermia does not improve long-term outcome [13, 45]. Serious adverse effects such as hypokalemia, atrial and ventricular arrhythmias, hypotension and coagulopathy may be associated with hypothermia [16].

#### **5.5 Glycemic control**

Hyperglycemia is associated with increased mortality in patients with TBI [46]. Target glycemic control between 4.4 to 6.7 mmol/L have been shown shortened hospital stay and improve outcome [47]. Hyperglycemia (> 11.1 mmol/L) is associated with 3.6 fold increased risk of mortality [48].

#### **5.6 Seizure prophylaxis**

Post-traumatic seizure (PTS) is a long-recognized and debilitating complication after traumatic brain injury [49, 50]. PTS are classified into immediate PTS (occurring within 24 hours of injury), early PTS (occurring within 7 days after injury), and late PTS (occurring after 7 days of post injury) [51]. Seizures can exacerbate intracranial hypertension by increasing cerebral blood flow corresponding with the need of brain oxygen and glucose [52, 53]. Continuous video recording of Encephalography (EEG) can be used as a diagnosis tools for PTS after TBI [54].

Seizure prophylaxis is recommended during the first week after TBI, particularly in high-risk patients such as those who have GCS scores <10; cortical contusion; depressed skull fracture; subdural, epidural, or intracerebral hematoma; penetrating head trauma; or seizures occurring within the first 24 hours after injury [5, 55]. The Brain Trauma Foundation Guidelines recommended the use of phenytoin in early PTS [16, 56, 57].

#### **5.7 Hyperventilation**

Hyperventilation is an effective and rapid method of treating intracranial hypertension. In the setting of intracranial hypertension, the goal of PaCO2 should

#### *Management of Traumatic Brain Injury DOI: http://dx.doi.org/10.5772/intechopen.98981*

be lower to 30 mmHg or 25–30 mmHg in extreme cases [13]. Reduction of PCO2 acutely induces vasoconstriction of cerebral arterioles and a decrease in cerebral blood volume, resulting in ICP reduction [19]. The effect supports within 30 minutes after hyperventilation, but generally lasts less than 24 h, due to buffering capacity of CSF compensations [16].

Both global and regional CBF are markedly decreased within 24 to 48 hours after head trauma [58]. Reduction of CBF in early phase of post injury is significantly associated with poor prognosis. Therefore, hyperventilation may have a role as a temporizing measure for the reduction of elevated ICP [59]. Meanwhile, SjvO2 or PbtO2 measurements can be used to monitor oxygen delivery [45, 59]. Hyperventilation should not be abruptly discontinued but should be tapered slowly over 4–6 h to avoid vasodilatation of cerebral arterioles and rebound increases in ICP [60].

#### **5.8 Hyperosmolar therapy**

Hyperosmolar therapy has critical role of medical treatment in acute intracranial hypertension by reducing brain volume. The most commonly used medications are mannitol and hypertonic saline (HS) [45].

Mannitol increase serum osmolality, resulting in an osmotic gradient from interstitial to intravascular space, reduction of cerebral edema and ICP. Mannitol also acts by other mechanisms, such as induction of reflex cerebral arteriolar vasoconstriction, improvement in blood rheology, reduction of CSF formation, and free radicals scavenging. The recommended ICP lowering dose of 20% mannitol is 0.25 to 1 g/kg every 6 hours [61]. Adverse effects of mannitol include acute renal failure, electrolyte disturbances and rebound of existing cerebral edema [62, 63].

Hypertonic saline (HS) is used alternatively to Mannitol and induce induction of reflex cerebral arteriolar vasoconstriction, improved deformability of erythrocytes with enhanced microcirculation, and an anti-inflammatory effect due to reduced adhesion of polymononuclear cells in the cerebral microvasculature [16]. Bolus and repeated doses are required until serum sodium level have been raised above normal (145–155 mEq/L) [64]. Possible adverse effects of HS include rebound cerebral edema, electrolyte disturbances (hypokalemia), congestive heart failure, renal failure, hyperchloremic metabolic acidosis, phlebitis, transient hypotension, hemolysis, osmotic demyelination, subarachnoid bleeding, seizures and muscle twitching [65].

#### **5.9 Sedation and analgesia**

Sedation and analgesia are an integral part of medical treatment. Patientventilator dyssynchrony and agitation increase intrathoracic pressure, which increase CBV and consequently increase ICP [27]. Ideal sedative drugs should have rapid onset and recovery for a quick neurological assessment, a predictable clearance independent of end organ failure and reducing cerebral blood flow and cerebral metabolic rate of oxygen consumption [11].

Opioids, benzodiazepines, propofol, barbituates and dexmedetomidine can be used to provide the sedation goal. The preferred regime is combination of an opioids such as fentanyl (1–3 μg/kg/hr) or sufentanil (0.1–0.6 μg/kg/hr) to provide analgesia and propofol (0.3–3 mg/kg/hr) for sedation [60]. According to the BTF guidelines, the administration of barbiturates is generally reserved for intracranial hypertension, refractory to maximum standard medical and surgical treatment [57].

Combination of nondepolarizing muscle relaxants and sedatives may be used during posturing, coughing, or agitation in head trauma care. When a neuromuscular blockade is used, EEG should be monitored to rule out convulsive states [66].

#### **5.10 Corticosteroids**

Recently, the BTF guidelines do not recommend the use of steroids for improving outcome or reducing ICP in TBI patients [59] because steroids are not effective in cytotoxic edema [60]. Steroid use is only indicated for reducing ICP in abscesses or neoplasms associated with vasogenic edema [60].

#### **5.11 Decompressive craniectomy (DC)**

Surgical removal of skull bone in effected side followed by evacuation of hematoma is considered if the patient deteriorating or ICP continues to rise [19]. Prompt removal of an acute subdural, epidural, or large solitary intracerebral hematoma is useful measure in traumatic brain injury treatment [67]. Decompressive craniectomy is risky and adverse effects are common. The complications are weighted against the life-threatening circumstances under which surgery is performed [68].

#### **5.12 Cerebrospinal fluid (CSF) drainage**

Procedure of CSF removal via external ventricular drainage device, lumbar drain or serial lumbar puncture is simple and tends to reduce intracranial pressure [16, 19]. Use of CSF drainage during the first 12 hours after injury may be considered in patients with an initial GCS <6 [57]. The major risks of EVD placement and CSF drainage include infection, hemorrhage and herniation [69].

#### **5.13 Other measures**

Nutritional support is required to facilitate recovery and should be initiated seventh day of post injury is recommended to improve outcome [57]. Recent guidelines suggest that transgastric jejunal feeding is recommended to reduce the incidence of ventilator associated pneumonia [59].

Proton-pump inhibitors, pantoprazole, 40 mg daily is suggested for stress ulcer prophylasix in critical care settings [70].

Supporting with pneumatic compression devices and use of LMWH or low-dose unfractioned heparin should be initiated as soon as possible for prophylaxis against deep venous thrombosis (DVT) [57]. The benefit of using heparin is considered to outweigh the risk of intracranial hemorrhage.

#### **Author details**

Soe Wunna Htay

Department of Anesthesiology and Critical Care, May Myo Military Hospital, Mandalay, Myanmar

\*Address all correspondence to: swunnah@gmail.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Management of Traumatic Brain Injury DOI: http://dx.doi.org/10.5772/intechopen.98981*

#### **References**

[1] Stelmasiak, Z., A. Dudkowska-Konopa, and K. Rejdak, Head trauma and neuroprotection. Medical Science Monitor, 2000. 6(2): p. RA426-RA432.

[2] Liew, B., et al., Early management of head injury in adults in primary care. Malaysian family physician: the official journal of the Academy of Family Physicians of Malaysia, 2017. 12(1): p. 22.

[3] Mena, J.H., et al., Effect of the modified Glasgow Coma Scale score criteria for mild traumatic brain injury on mortality prediction: comparing classic and modified Glasgow Coma Scale score model scores of 13. The Journal of trauma, 2011. 71(5): p. 1185.

[4] Aitkenhead, A.R., et al., Smith and Aitkenhead's Textbook of Anaesthesia E-Book: Expert Consult-Online & Print. Neurosurgical Anesthesia. Vol. Sixth Edition. 2013: Elsevier Health Sciences. pp 654-656.

[5] Cottrell, J.E. and W.L. Young, Cottrell and Young's neuroanesthesia. Care of Acutely Unstable Patient. Vol. Fifth Edition. 2016: Elsevier Health Sciences. 161-169.

[6] Lev, R. and P. Rosen, Prophylactic lidocaine use preintubation: a review. The Journal of emergency medicine, 1994. 12(4): p. 499-506.

[7] Turner, B.K., et al., Neuroprotective effects of thiopental, propofol, and etomidate. AANA journal, 2005. 73(4): p. 297.

[8] Muñoz-Martínez, T., et al., Contraindications to succinylcholine in the intensive care unit. A prevalence study. Medicina intensiva, 2014. 39(2): p. 90-96.

[9] Tran, D., et al., Rocuronium vs. succinylcholine for rapid sequence intubation: a Cochrane systematic review. Anaesthesia, 2017. 72(6): p. 765-777.

[10] Videtta, W., et al., Effects of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure, in Intracranial Pressure and Brain Biochemical Monitoring. 2002, Springer. p. 93-97.

[11] Peluso, L., B.M. Lopez, and R. Badenes, Sedation in TBI Patients, in Traumatic Brain Injury-Neurobiology, Diagnosis and Treatment. 2019, IntechOpen.

[12] Hutchison, J.S., et al., Impact of hypotension and low cerebral perfusion pressure on outcomes in children treated with hypothermia therapy following severe traumatic brain injury: a post hoc analysis of the Hypothermia Pediatric Head Injury Trial. Developmental neuroscience, 2010. 32(5-6): p. 406-412.

[13] Ragland, J. and K. Lee, Critical care management and monitoring of intracranial pressure. Journal of Neurocritical Care, 2016. 9(2): p. 105-112.

[14] Nag, D.S., et al., Intracranial pressure monitoring: Gold standard and recent innovations. World journal of clinical cases, 2019. 7(13): p. 1535.

[15] Abraham, M. and V. Singhal, Intracranial pressure monitoring. Journal of Neuroanaesthesiology and Critical Care, 2015. 2(03): p. 193-203.

[16] Schizodimos, T., et al., An overview of management of intracranial hypertension in the intensive care unit. Journal of Anesthesia, 2020. 34: p. 741-757.

[17] Ristic, A., R. Sutter, and L.A. Steiner, Current neuromonitoring techniques in critical care. Journal of Neuroanaesthesiology and Critical Care, 2015. 2(02): p. 097-103.

[18] Rajajee, V., et al., Optic nerve ultrasound for the detection of raised intracranial pressure. Neurocritical care, 2011. 15(3): p. 506-515.

[19] Sadoughi, A., I. Rybinnik, and R. Cohen, Measurement and management of increased intracranial pressure. The Open Critical Care Medicine Journal, 2013. 6(1).

[20] Gwer, S., et al., The tympanic membrane displacement analyser for monitoring intracranial pressure in children. Child's Nervous System, 2013. 29(6): p. 927-933.

[21] Tasneem, N., et al., Brain multimodality monitoring: a new tool in neurocritical care of comatose patients. Critical care research and practice, 2017. 2017.

[22] Le Roux, P., et al., Consensus summary statement of the international multidisciplinary consensus conference on multimodality monitoring in neurocritical care. Neurocritical care, 2014. 21(2): p. 1-26.

[23] Kurtz, P., K.A. Hanafy, and J. Claassen, Continuous EEG monitoring: is it ready for prime time? Current opinion in critical care, 2009. 15(2): p. 99-109.

[24] Peacock, S.H. and A.D. Tomlinson, Multimodal neuromonitoring in neurocritical care. AACN advanced critical care, 2018. 29(2): p. 183-194.

[25] Frost, E.A., Essentials of Neuroanesthesia and Neurointensive Care. Anesthesia and Analgesia, 2009. 108(2): p. 678-679.

[26] Capatina, C., et al., Diabetes insipidus after traumatic brain injury. Journal of clinical medicine, 2015. 4(7): p. 1448-1462.

[27] Godoy, D.A., S. Lubillo, and A.A. Rabinstein, Pathophysiology and management of intracranial hypertension and tissular brain hypoxia after severe traumatic brain injury: an integrative approach. Neurosurgery Clinics, 2018. 29(2): p. 195-212.

[28] Frost, E.A., Effects of positive end-expiratory pressure on intracranial pressure and compliance in brain-injured patients. Journal of neurosurgery, 1977. 47(2): p. 195-200.

[29] Robertson, C.S., Management of cerebral perfusion pressure after traumatic brain injury. The Journal of the American Society of Anesthesiologists, 2001. 95(6): p. 1513-1517.

[30] Smith, M., Cerebral perfusion pressure, in BJA: British Journal of Anaesthesia. 2015, Oxford University Press: Lhttps://doi.org/10.1093/bja/ aev230ondon. p. Pages 488-490.

[31] Prabhakar, H., et al., Current concepts of optimal cerebral perfusion pressure in traumatic brain injury. Journal of anaesthesiology, clinical pharmacology, 2014. 30(3): p. 318.

[32] Nordström, C.-H., Physiological and biochemical principles underlying volume-targeted therapy—the "Lund concept". Neurocritical care, 2005. 2(1): p. 83-95.

[33] Alvis-Miranda, H.R., S.M. Castellar-Leones, and L.R. Moscote-Salazar, Intravenous fluid therapy in traumatic brain injury and decompressive craniectomy. Bulletin of Emergency and Trauma, 2014. 2(1): p. 3.

*Management of Traumatic Brain Injury DOI: http://dx.doi.org/10.5772/intechopen.98981*

[34] De Backer, D. and J.-L. Vincent, Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions. Critical Care, 2018. 22(1): p. 1-6.

[35] Zornow, M.H. and D.S. Prough, Fluid management in patients with traumatic brain injury. New Horiz, 1995. 3(3): p. 488-98.

[36] Alvis-Miranda, H.R., et al., Fluid therapy in neurotrauma: basic and clinical concepts. Reviews in Health Care, 2014. 5(1): p. 7-22.

[37] Thompson, M., et al., Comparison of crystalloid resuscitation fluids for treatment of acute brain injury: a clinical and pre-clinical systematic review and network meta-analysis protocol. Systematic reviews, 2018. 7(1): p. 1-7.

[38] Zornow, M. and D. Prough, Fluid management in patients with traumatic brain injury. New horizons (Baltimore, Md.), 1995. 3(3): p. 488-498.

[39] Kozek-Langenecker, S.A., Effects of hydroxyethyl starch solutions on hemostasis. The Journal of the American Society of Anesthesiologists, 2005. 103(3): p. 654-660.

[40] Badenes, R., et al., Hemoglobin concentrations and RBC transfusion thresholds in patients with acute brain injury: an international survey. Critical care, 2017. 21(1): p. 1-10.

[41] Lelubre, C., et al., Anemia management after acute brain injury. Critical care, 2016. 20(1): p. 1-11.

[42] Schulz-Stübner, S. and R. Thiex, Raising the head-of-bed by 30 degrees reduces ICP and improves CPP without compromising cardiac output in euvolemic patients with traumatic brain injury and subarachnoid haemorrhage: a practice audit. European Journal of

Anaesthesiology (EJA), 2006. 23(2): p. 177-180.

[43] Gholamzadeh, S., et al., Examination of the effect of lidocaine on intracranial pressure during endotracheal suctioning in severe head-injured patients in Shiraz-Iran: P 089. European Journal of Anaesthesiology| EJA, 2008. 25: p. 31.

[44] Greer, D.M., et al., Impact of fever on outcome in patients with stroke and neurologic injury: a comprehensive meta-analysis. Stroke, 2008. 39(11): p. 3029-3035.

[45] Stocchetti, N. and A.I. Maas, Traumatic intracranial hypertension. New England Journal of Medicine, 2014. 370(22): p. 2121-2130.

[46] Shi, J., et al., Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor. Oncotarget, 2016. 7(43): p. 71052.

[47] Hermanides, J., et al., Glycaemic control targets after traumatic brain injury: a systematic review and metaanalysis. Critical Care, 2018. 22(1): p. 1-11.

[48] Griesdale, D.E., et al., Glucose control and mortality in patients with severe traumatic brain injury. Neurocritical care, 2009. 11(3): p. 311.

[49] Evans, R.W. and S.C. Schachter, Post-traumatic seizures and epilepsy. UptoDate. Available from: https://www. uptodate.com/contents/post-traumaticseizures-and-epilepsy, 2014.

[50] Pingue, V., C. Mele, and A. Nardone, Post-traumatic seizures and antiepileptic therapy as predictors of the functional outcome in patients with traumatic brain injury. Scientific reports, 2021. 11(1): p. 1-12.

[51] Nichol, H., J. Boyd, and J. Trier, Seizure Prophylaxis Following Moderate to Severe Traumatic Brain Injury: Retrospective Investigation of Clinical Practice and the Impact of Clinical Guidelines. Cureus, 2020. 12(4).

[52] Marguc, K., et al., Measurements of CBF in Patients with Epilepsy, in Cerebral Blood Flow and Metabolism Measurement. 1985, Springer. p. 202-204.

[53] Posner, J.B., F. Plum, and A. Van Poznak, Cerebral metabolism during electrically induced seizures in man. Archives of Neurology, 1969. 20(4): p. 388-395.

[54] Piccenna, L., G. Shears, and T.J. O'Brien, Management of post-traumatic epilepsy: An evidence review over the last 5 years and future directions. Epilepsia open, 2017. 2(2): p. 123-144.

[55] Ding, K., P.K. Gupta, and R. Diaz-Arrastia, Epilepsy after traumatic brain injury. Translational research in traumatic brain injury, 2016.

[56] Fordington, S. and M. Manford, A review of seizures and epilepsy following traumatic brain injury. Journal of neurology, 2020. 267: p. 3105-3111.

[57] Carney, N., et al., Guidelines for the management of severe traumatic brain injury. Neurosurgery, 2017. 80(1): p. 6-15.

[58] Stocchetti, N., et al., Hyperventilation in head injury. Chest, 2005. 127(5): p. 1812-1827.

[59] Bullock, M. and J. Povlishock, Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, AANS/CNS Joint Section on Neurotrauma and Critical Care. Guidelines for the management of severe traumatic brain injury. J Neurotrauma, 2007. 24(suppl 1): p. S1-106.

[60] Mayer, S.A. and J.Y. Chong, Critical care management of increased intracranial pressure. Journal of Intensive Care Medicine, 2002. 17(2): p. 55-67.

[61] Shawkat, H., M.-M. Westwood, and A. Mortimer, Mannitol: a review of its clinical uses. Continuing education in anaesthesia, critical care and pain, 2012. 12(2): p. 82-85.

[62] Shi, J., et al., Hypertonic saline and mannitol in patients with traumatic brain injury: A systematic and metaanalysis. Medicine, 2020. 99(35).

[63] Schwimmbeck, F., et al., Hypertonic saline versus mannitol for traumatic brain injury: a systematic review and meta-analysis with trial sequential analysis. Journal of neurosurgical anesthesiology, 2021. 33(1): p. 10-20.

[64] Ennis, K.M. and G.M. Brophy, Management of intracranial hypertension: Focus on pharmacologic strategies. AACN advanced critical care, 2011. 22(3): p. 177-182.

[65] Georgiadis, A.L. and J.I. Suarez, Hypertonic saline for cerebral edema. Current neurology and neuroscience reports, 2003. 3(6): p. 524-530.

[66] Shapiro, H.M., Intracranial hypertension: therapeutic and anesthetic considerations. The Journal of the American Society of Anesthesiologists, 1975. 43(4): p. 445-471.

[67] Nakagawa, K. and W.S. Smith, Evaluation and management of increased intracranial pressure. CONTINUUM: Lifelong Learning in Neurology, 2011. 17(5): p. 1077-1093.

[68] Stiver, S.I., Complications of decompressive craniectomy for traumatic brain injury. Neurosurgical focus, 2009. 26(6): p. E7.

*Management of Traumatic Brain Injury DOI: http://dx.doi.org/10.5772/intechopen.98981*

[69] Grady, M.S., Lumbar drainage for increased intracranial pressure. Journal of neurosurgery, 2009. 110(6): p. 1198-1199.

[70] Ye, Z., et al., Gastrointestinal bleeding prophylaxis for critically ill patients: a clinical practice guideline. Bmj, 2020. 368.

### Section 5

## Acute Compartment Syndrome

#### **Chapter 7**

## Acute Compartment Syndrome of the Extremities and Paraspinal Muscles

*Balaji Zacharia and Raj Vignesh Selvaraj*

#### **Abstract**

Acute compartment syndrome (ACS) occurs when the pressure within the closed osteo-fascial compartment raises above perfusion pressure leading to irreversible tissue ischemia and necrosis. Any closed compartment in the body can be affected by ACS. The leg is the commonest site. Trauma is the common cause of compartment syndrome in young patients. In older patients, medical causes can cause it. The diagnosis in a conscious patient can be made based on clinical features. Pain out of proportion to the injury is the most important symptom. Exacerbation of pain on stretching the affected muscles and paresthesia are the common signs. Compartment pressure measurement is important for the diagnosis in unconscious and uncooperative patients. The treatment of established ACS is emergency fasciotomy. Untreated compartment syndrome can lead to neurovascular injuries and muscle contractures. In this chapter, we will see the etiologies, clinical features, investigations, and management of acute compartment syndrome of the extremities and the paraspinal region.

**Keywords:** acute compartment syndrome, compartment syndrome of extremities, compartment syndrome of paraspinal muscles

#### **1. Introduction**

Compartment syndrome is a condition where the pressure within the closed osteo-fascial compartment raises above the perfusion pressure leading to irreversible tissue ischemia and necrosis. A decrease in the compartment volume, an increase in the contents of the compartment, or external pressure can cause it. The compartment syndrome can be acute or chronic. Untreated acute compartment syndrome (ACS) can cause cosmetic problems due to muscle contractures, and functional problems due to neurovascular damages. These can be reasons for litigations against treating doctors. If detected early and treated properly most of the sequelae of ACS are preventable [1]. In 1881 Dr.Richard von Volkmann a German doctor first described ACS [2]. Paul Jepson in 1924 demonstrated ischemic contracture of muscles in animals [10]. The incidence of ACS is 0.7 to 7.3 persons per 100,000 people [3]. The leg is the most common site of ACS. About 2–9% of fractures of the tibia are associated with ACS [4]. There is an equal incidence of ACS in closed and open fractures [5]. A higher incidence of ACS is seen in grade 2 compound fractures than in grade 3A or 3B due to the phenomenon of self-decompression seen in higher grade open injuries. Due to the bulk of muscles attached to the diaphysis of long bones, fractures through

diaphysis are prone to develop ACS [6]. The forearm, hands, feet, buttocks, thighs, and paraspinal muscles are other sites. Any closed fascial space can be affected [7]. There can be fracture-related and non- fracture-related ACS. Fracture-related ACS is common in young males and its diagnosis is early. Whereas non- fracture-related ACS is common in the elderly with medical comorbidities. The ACS in the elderly can be traumatic or nontraumatic. The posterior compartment of the leg is affected commonly in non-fracture-related ACS group. In older people with swollen limbs, a compartment pressure measurement is needed to rule out ACS [8].

#### **1.1 Etiologies**

Most cases of ACS occur following trauma. Young males are about ten times more affected than females. Other than fractures there are many other etiologies. Arterial injuries, snake bite, burns, gunshot injuries, leakage from arterial and venous access, drug overdose, pulsatile lavage, contusions in hemophilia, infection, and intraosseous fluid replacement in infants are other causes for acute compartment syndrome. Over-exertion can lead to acute or chronic compartment syndrome. Lithotomy positioning during surgery or constricting casts or wraps can cause it. ACS can also occur due to non-traumatic medical conditions like nephrotic syndrome, viral myositis, hypothyroidism, bleeding disorders, malignancies, diabetes mellitus (Diabetes –associated muscle infarction), and in rheumatological conditions like ruptured Baker's cyst [9].

An awareness regarding the etiology, pathophysiology, clinical features, investigations and management is essential for all doctors dealing with patients in the emergency department. In this narrative review, we intend to give a detailed overview of acute compartment syndrome.

#### **2. Anatomy of the compartments**

The major groups of muscle and neurovascular structures are separated by a thick layer of fascia. The fascia provides a surface for the attachment of muscles and keeps the contour of the muscles. It improves mechanical advantage during contractions. The fascia helps in coordinated actions of muscle and proprioception. These fasciae divide the extremity into different compartments.

There are 4 compartments in the leg. They are anterior, lateral, superficial, and deep posterior compartments. The anterior intermuscular septum separates the lateral muscles from the anterior muscles, and the posterior intermuscular septum separates the lateral muscles from the posterior muscles. The interosseous membrane spans the gap between the tibia and fibula, separating the anterior and deep posterior compartments. The transverse intermuscular septum separates the musculature of the superficial and deep posterior compartments. The anterior compartment contains the anterior tibial artery and veins, deep peroneal nerve. Tibialis anterior, extensor hallucis longus, and extensor digitorum longus are the muscles in this compartment. Peroneus longus and peroneus brevis muscles with superficial peroneal nerves are in the lateral compartment. The superficial posterior compartment contains gastrocnemius, soleus, and plantaris muscles. The peroneal vessels, posterior tibial vessels, tibial nerve and tibials posterior, flexor digitorum longus, and flexor hallucis longus muscles are the contents in the deep posterior compartment of the leg [10].

There are controversies regarding the actual number of compartments in the foot. Various authors reported three to nine compartments in the foot. The medial, lateral, and superficial compartments run along the entire length of the foot. The

#### *Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

four interossei and an adductor compartment are confined to the forefoot. Manoli and Weber described a calcaneal compartment containing quadratus Plantae muscle, posterior tibial, and lateral plantar vessels and nerves. The medial compartment contains abductor hallucis brevis, and flexor hallucis brevis, and lateral compartment abductor digiti quinti and flexor digiti quinti. Flexor digitorum brevis and lumbrical muscles in the superficial compartment [11].

The forearm is divided into three compartments volar dorsal and lateral. The interosseus membrane separates the volar and dorsal compartments. The lateral compartment containing the mobile wad muscles is separated by the antebrachial septum is lying in the posterior and lateral part. Volar muscles are commonly affected in ACS. There is anatomical communication between various compartments of the forearm so the release of the volar compartment alone can reduce pressure in others [12]. The thenar, hypothenar, adductor, and interosseous compartments are the main osteo-fascial compartments of the hand [13].

The anterior, medial, and posterior are the fascial compartments in the thigh. The lateral intermuscular septum is very tough whereas the medial and posterior septum is thinner. The hamstrings are in the posterior compartment, adductors in the medial, and quadriceps in the anterior compartments. There is a lot of potential space in the thigh compartments before the elevation of intra compartmental pressure [14].

#### **3. Pathophysiology**

ACS is due to elevation of interstitial pressure due to any reason. The difference between interstitial pressure and capillary perfusion pressure (CPP) is the determinant of tissue perfusion. When the volume of an osteo-fascial compartment increases as in intra-compartment bleeding due to injury, both tissue and venous pressure increases. Once this pressure exceeds CPP there is a collapse of capillaries resulting in ischemia of muscles and nerves. This can happen due to external compression also. This is the arteriovenous pressure gradient theory for the development of ACS [15]. A vicious cycle follows that (Appendix 1). The decreased capillary pressure leads to decreased tissue perfusion leading to increased capillary permeability and increased extravasation of fluid into the interstitial spaces further increasing the tissue pressure and decrease in tissue perfusion. A decrease in venous return also results in a decrease in tissue perfusion due to an increase in interstitial pressure [16]. When the intra-compartment pressure is more than 10 to 30 mm of Hg above the diastolic pressure tissue perfusion is compromised, and when it exceeds mean arterial pressure muscle ischemia starts. There is a direct relation between systemic blood pressure and intra-compartmental pressure in the development of ACS. Hence a hypotensive patient is more likely to develop ACS compared to normotensive [17].

Most muscle injury occurs not during the phase of ischemia but at the time of reperfusion. Ischemia–reperfusion syndrome is the cellular and systemic effects of ischemia followed by reperfusion. Normally the energy demands are met by oxidation of free fatty acids leads to aerobic conversion of ADP to ATP. During ischemia, cells try to preserve energy. Ischemia induces two anaerobic pathways for energy production. The first is from creatine phosphate stored in the muscles. The creatine kinase in the muscle produces a large amount of ATP by transferring phosphate from creatine phosphate to the ADP molecule. The creatine phosphate stores in the muscles will be depleted within three hours. The glycogen within the muscles is the next source of energy. The glycogen is broken down into pyruvate and lactate. The hydrogen ions released during this process decrease the intracellular pH. This inhibits glycolysis by negative inhibition of the rate-limiting enzyme phosphofructokinase. This is an inefficient mechanism of ATP production. This will end in six hours. Later dephosphorylation of adenosine nucleotide continues leading to the production of fat-soluble precursors like inosine monophosphate, adenosine, hypoxanthine, and xanthine. These products are washed away during reperfusion and unavailable for adenine nucleotide restoration. The vasodilation during revascularization leads to hyperemia to the extremity. This will wash away the lactate and precursors of adenine nucleotide metabolism. The hyperemia causes increased extravasation fluid through the capillaries leading to a rise in interstitial pressure. The muscles are the only tissue in which xanthene dehydrogenase is converted to xanthine oxidase during reperfusion and not during ischemia. This is due to the increased concentration of cytosolic calcium. The oxygen-free radicles produced by the xanthene oxidase react with proteins and enzymes. The free radicles attack the unsaturated bonds of free fatty acids in the phospholipid bilayer of the cell membrane called lipid peroxidation. Lipid peroxidation causes fragmentation and structural-functional alteration in the membrane leading to increased permeability. This reaction in the capillary leads to increased permeability cell swelling and interstitial edema increasing the vascular resistance. These abnormalities in the cell wall functions allow calcium influx into the cytoplasm. Increased cytoplasmic calcium will completely uncouple the oxidative phosphorylation and production of ATP in the mitochondria. This influx of calcium leads to cell death and necrosis. This reperfusion injury cascade can induce further local and systemic organ failure [18].

The irreversible changes and reduction of aerobic metabolism in the tissue due to ischemia are different for different tissues. It depends on the ischemic time which can vary from minutes to hours. Within 6 hours of acute ischemia irreversible tissue necrosis and inflammatory cascade leading to fibrosis sets in muscles. Ischemia of 1 hour produces reversible neuropraxia in nerves. Irreversible axonotmesis sets in about 4 hours of acute ischemia [19, 20].

#### **4. Clinical features**

The signs and symptoms of ACS evolve within few hours. A high index of suspicion is required for the diagnosis of ACS. Griffiths described pain, paresthesia, paresis, and pain with stretch as the main symptoms of ACS ("four Ps") later pulselessness and pink color of skin were added [21, 22]. Pain out of proportion to the known injury is the earliest symptom. Pain not responding to analgesics also make us suspicious. Resting pain and exacerbation of pain on passive stretching of affected muscles are present. Paresthesia due to ischemia of nerves can be an early sign. But an assessment of neurological functions for the diagnosis of ACS can be tricky. The extreme pain, anxiety, and altered mental status due to an injury can make proper neurological examination impossible. The motor nerve fibers can withstand the ischemia to a longer extent than sensory fibers hence motor weakness will be present at a later stage. Swelling and distension of the affected extremity should alert the surgeon about the possibility of an incumbent ACS. Resting pain or pain due to passive stretching of muscles, paresthesia, pallor, pulselessness, and paresis (5Ps) can be seen in ACS. Any one of the above signs may not be indicative of ACS. When three or more of the above signs are present in combination in a patient at risk of developing ACS will increase the sensitivity of these signs for diagnosis. Among these signs, the paresis may take longer to appear. The 5 Ps described above are characteristic features of arterial ischemia. In a conscious patient pain out of proportion to known injuries and paresthesia are the most important signs. Two-point discrimination is a more sensitive test than a light touch. Sometimes a 6th P - Poikilothermia a change in temperature of the extremity or coolness of

#### *Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

the affected limb may be present in ACS [23]. In young children with injury, the above-mentioned features may not be useful for diagnosis. They may not be able to communicate regarding their symptoms and signs. The increasing need for analgesics, features of agitation, and anxiety (3 As) are indicators for the development of ACS. Clinical diagnosis of ACS is challenging in an unconscious patient, in a patient using patient-controlled analgesia, regional anesthesia, and use of epidural pain catheters because of masking of clinical features [24].

The leg is the most common site of acute compartment syndrome. The anterior and lateral compartments of the leg are commonly affected. Fractures of the tibia, tibial plateau fractures, and fracture-dislocations of the knee are the common injuries producing ACS of the leg. According to the compartment involved the clinical features can change. Paresthesia of the first webspace of the foot is an early sign. Later weakness of dorsiflexion of the great toe, inversion of the foot, and dorsiflexion of the ankle are seen in anterior compartment involvement. The lateral compartment syndrome produces a sensory loss in the dorsolateral aspect of the foot with weakness of eversion of the foot. Deep posterior compartment involvement leads to loss of plantar flexion of the toes with loss of sensations in the plantar aspect of the foot. Plantar flexion of the ankle will be weak when the superficial posterior compartment is affected [25].

Dislocations of Chopart and Lisfranc joints are the commonest cause for foot compartment syndrome. Isolated fractures of the mid-foot bones are a very rare cause. The symptoms are similar to leg compartment syndrome. Frequent checking of sensations especially two-point discrimination is a sensitive test. Passive stretching of muscles results in exacerbation of pain [26].

ACS of the thigh is a very rare and potentially devastating condition. Fracture of the shaft of the femur, contusion, coagulopathy, vascular injuries, intramuscular hematoma, arthroplasties of hip and knee, and arthroscopy of the knee are some of the etiologies. The outcome can be an uneventful recovery to severe morbidity and mortality. The diagnosis of ACS in a conscious patient able to cooperate with examination is based on the following criteria. Pain out of proportion to the injury, significant swelling of the thigh, palpable induration of the involved compartment, increase in measured thigh circumference, pain with passive stretching, weakness of the involved muscle, sensory or motor weakness in the nerves in the affected compartment are all seen in varying combinations in acute compartment syndrome of the thigh. An excessively painful, tensely swollen thigh is the most consistent finding of ACS of thigh [27].

The lumbar paraspinal muscle compartment syndrome can be either acute or chronic. Acute cases are due to injuries from downhill skiing, or surfing, direct injury to muscles, or lifting weight. Localized paraspinal muscle tenderness, board-like rigidity of the muscles, deep tenderness on palpation of the abdomen, absent bowel sounds, and loss of sensation over the paraspinal area are the common features. Localized loss of sensations in the paraspinal region is a pathognomonic finding [28].

Supracondylar fracture of the humerus with vascular injury is the commonest cause of ACS in the forearm. The deep volar compartment is commonly involved, flexor pollicis longus and flexor digitorum profundus are commonly involved. Trauma, crush injuries, insect bites are the commonest cause of ACS of hand. Other than the usual symptoms and signs pain on passive motion of the metacarpophalangeal joints of the corresponding intrinsic muscle is a sensitive test [29, 30].

#### **5. Investigations**

Despite the awareness among doctors about the possibility of ACS in trauma patients it is one condition frequently missed leading to devastating complications. The clinical suspicion of this condition must lead to immediate decompression

without many investigations. This is especially true in an unconscious patient, intubated patients, and who cannot respond appropriately.

The compartment pressure measurement is the most common method used to diagnose ACS. The measurement of pressure should be done within 5cms from the fracture and not at the site of fracture. Compartment pressure measured over time is more useful than a single measurement. The diagnosis depends on the delta pressure measurement. Delta pressure is the difference between diastolic pressure and compartment pressure. When delta pressure is equal to or less than 30 mg of Hg it indicates ACS. If we use only delta pressure for treatment it has been shown that many asymptomatic patients will undergo fasciotomy. So diagnosis must be confirmed only with clinical findings and hemodynamic and metabolic parameters [31]. In an unconscious patient compartment pressure measurement is the only way to diagnose ACS. Compartment pressure must be checked every 4 hours in the first 24 hours in all high-risk unconscious patients after an injury.

Several techniques can be used for measuring compartment pressure. The needle manometry technique is the simplest and cheapest technique. This is introduced by whitesides et al. (1975). The Wick catheter, the slit catheter, the solid-state transducer intra- compartment catheter, myopress catheter, and transducer-tipped fiber optic catheters are other methods used [32].

The intramuscular partial pressure of oxygen can be measured noninvasively using Near-Infrared spectroscopy (NIRS). There is an increase in perfusion to the injured site. So the partial pressure of oxygen will increase at the site of injury. If there is no increase in the partial pressure of oxygen at the site of injury it can indicate ACS. This is the principle of NIRS. The intramuscular partial pressure of oxygen can vary among individuals and different compartments. A comparison of the NIRS value of the same compartment of the opposite uninjured leg is a useful tool for diagnosis. There is some controversy regarding the use of NIRS for the monitoring of ACS. Different factors like depth of tissues, discoloration of the skin, a hematoma can interfere with the results of NIRS [33].

Many different techniques are used for detecting compartment pressure and perfusion but they are still in the development or experimental stage. Ultrasonography can show increased echogenicity of the compartment when pressure increases. It can also be used to detect changes in elasticity when standardized external pressure is applied. Both techniques are in an experimental stage. Pulse Phased Locked Loop (PPLL) ultrasound is useful in detecting the displacement of fascia with arterial pulsation. This technique was found to be useful to detect raised compartment pressure in cadaveric studies. Photoplethysmography, laser Doppler flowmetry, and scintigraphy, intramuscular glucose monitoring are all used to find out raised compartment pressure. They are not used widely in clinical practice [34].

The serum biomarkers are used for the diagnosis of ACS without many shreds of evidence. Elevated Troponin Levels and myoglobinuria can assist in the diagnosis of ACS. There are also reports suggesting the usefulness of lactate levels from femoral veins in the diagnosis of ACS in patients with femoral artery injury. Serum biomarkers are not useful in the delayed diagnosis of ACS [35]. The creatine kinase level increases during ACS. Creatine kinase level > 1000 U/ml or myoglobinuria are suggestive of ACS. There are abnormalities in renal function tests and hyperkalemia due to rhabdomyolysis [36].

#### **6. Treatment**

Acute compartment syndrome is a surgical emergency. If not diagnosed early and treated promptly it can lead to devastating complications. The sequel of untreated

#### *Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

or mismanaged ACS includes unacceptable deformities, neurological injuries, crush syndrome, renal failure, limb amputation, and death. There are certain preventive measures that we should do to prevent the development of acute compartment syndrome in all patients with limb injuries. All circumferential and tight bandages should be removed. Split tight plaster cast. The Limb should be kept at heart level. Avoid patient going into hypotension, and maintain oxygen saturation. These measures reduce the risk of the development of ACS in high-risk patients.

The treatment of ACS is emergency decompression of the compartment. The fasciotomy is used for decompression. Fasciotomy should be done within 6 hours or definitely within 12 hours after diagnosis of ACS. Fasciotomy must be done in all patients with clinical findings of ACS when compartment pressure is more than 30 mm of Hg, and when delta pressure is less than or equal to 30 mm of Hg. The fasciotomy should be liberal decompressing all the compartments of the limb including the epimysium to relieve integumental compartment pressure. In the legs all 4 compartments, and the forearm, both dorsal and volar compartments should be decompressed. The fasciotomy wound can be closed by delayed primary intension, or by a split-thickness skin graft. The use of negative pressure wound therapy for fasciotomy wounds is controversial. It can help to reduce the swelling and early closure of wounds or skin grafting. A fasciotomy is not indicated when there is irreversible intra-compartmental damage like neuromuscular or vascular damage in an adult patient. If fracture fixation is needed in such a patient either external fixation or plaster cast can be used without violating the affected compartment. In a patient with ACS fracture fixation, either internal or external fixation can be done along with fasciotomy [35, 37]. In children, delayed fasciotomies have shown better outcomes than adults. We can do fasciotomies up to 24 hours after injury in children [38].

ACS of the leg is common in the fractures of the diaphysis, proximal fracture of tibia with comminution, long periarticular fragments, fracture-dislocations, and medial tibial condyle fractures. Comminuted fracture of the fibula at the same level of fracture of tibia is also associated with a high incidence of ACS [39].

All four compartments have to be decompressed. The commonly used 2 incision technique involves a longitudinal incision on the posteromedial aspect of the leg extending from the proximal tibia to distally up to the musculotendinous junction of the gastro-soleus muscle. The incision is made 2 cm posterior to the posteromedial corner of the tibia. Care should be taken to avoid injuring the sural nerve proximally and saphenous vein distally. The fascia is incised in line with incision decompressing the superficial compartment. The deep compartment is decompressed by elevating the soleus muscle and cutting the fascia covering it. We can extend the incision proximally and distally as needed for the release. The second incision is made 2 cm anterior to the head of the fibula. The incision extends from the head of the fibula to the distal fibula. The anterior skin flap is raised and the lateral intermuscular septum is identified and the anterior compartment is released by incising the entire length of the facia from proximal to distal. The superficial peroneal nerve is at risk at the distal third. The lateral compartment is released by incising the fascia along the posterior border of the fibula (**Figure 1**) [40].

A single incision technique can be used for the fasciotomy of the leg. A longitudinal incision is made along the entire length of the fibula. A transverse incision is made to identify the lateral intermuscular septum then decompression of the anterior and lateral compartment is done. The posterior compartment is decompressed after elevating the attachment of the soleus from the fibula and then identifing the posterior compartment and decompressing it. Fibulectomy can be used to decompress all 4 compartments of the leg, but it should be avoided especially in patients with complex tibial fractures [41].

**Figure 1.** *Diagram showing the compartments of the leg and arrows 1 & 2 represent the approach for the fasciotomy of the leg.*

There are different methods for fasciotomy of the foot. The most commonly used method is a combination of medial and dorsal approaches. The dorsal approach involves two longitudinal incisions one medial to the second metatarsal and another lateral to the fourth metatarsal. There should be adequate space between these 2 incisions to prevent necrosis of the skin. The medial incision is about 6 cm long starting from about 4 cm anterior to heel and about 3 cm above the plantar surface of the foot. The dorsal approach helps to decompress the interossei and adductor compartments (**Figure 2**). The medial approach releases the medial, superficial, calcaneal, and lateral compartments [42].

**Figure 2.** *Dorsal approach for fasciotomy of the foot- a cross-section.*

#### *Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

The decompression of all three compartments is indicated in ACS of the thigh. The anterior and posterior compartments are decompressed using a single lateral incision extending from the intertrochanteric line to the lateral epicondyle of the femur. The skin and subcutaneous tissue are opened along the skin incision. The iliotibial band is identified. By dividing the iliotibial band fascia covering the vastus lateralis the anterior compartment is released. The posterior compartment is opened after retracting the vastus lateralis and dividing the intermuscular septum. The medial compartment is decompressed using a separate longitudinal medial incision and dividing the medial intermuscular septum (**Figure 3**) [43].

The paraspinal muscles are enclosed in the thoracolumbar fascia which acts as a closed fascial compartment. It covers the muscles from all sides except medially where it is attached to the spinous process and interspinous ligaments (**Figure 4**). Surgical release of the thoracolumbar fascia gives better results than nonoperative treatment in the compartment syndrome of the paraspinal muscles. There is no consensus regarding the timing of fasciotomy. Most reports agree on fasciotomy within 7 days. The approach is Wiltse paraspinal incision. The thoracolumbar fascia is divided and individual muscle compartments are released [44].

The management of ACS of the forearm involves decompression of the compartment using volar and dorsal approaches. The volar incision is curvilinear. It extends from proximal and medal to cubital fossa then extends distally along the radial side of the forearm till the distal third. Then again it is curved medially to the midline of the forearm over the wrist for release of carpal tunnel (**Figure 5**). This incision helps to decompress the median nerve and helps to cover the median nerve using the radial flap. The lacertus fibrous is released and the superficial volar compartment is released. The identification of the deep fascia and its release is very important. The pronator quadratus should be identified and its fascia should be released separately. The dorsal compartment is decompressed using a single midline incision

#### **Figure 3.**

*The anterior, lateral, and posterior compartments of the thigh and arrows representing the lateral and medial fasciotomy approaches.*

#### **Figure 4.**

*Diagram showing the paraspinal muscle compartment, the thoracodorsal fascia covering the muscles all around and medially to the spinous process and interspinous ligaments.*

**Figure 5.** *The volar approach for fasciotomy of the forearm.*

#### *Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

extending from lateral epicondyle to distal radioulnar joint. The individual septum separating the muscles should be released individually [45].

The hand compartment is released by the volar and dorsal approach. Dorsally decompression is done using 2 incisions along the 2nd and 4th metacarpals. The release is done on either side of the metacarpals to decompress the interossei. Deeper dissection along the radial aspect of the 2nd metacarpal is used for decompressing the adductor compartment. The volar incision is used to release the thenar and hypothenar compartments. The carpal tunnel should also be released [46].

#### **7. Conclusion**

Acute compartment syndrome is a surgical emergency. The diagnosis is based on clinical findings so careful history and physical examination are required. In obtunded patients, the diagnosis is made when delta pressure ≤ 30mm of Hg and compartment pressure > 30 mm of Hg. Emergency fasciotomy and decompression of the compartment is the treatment of choice. Usually, a repeat inspection of the fasciotomy wound after 24 to 48 hours should be done. Delayed closure of the wound is done.

#### **Appendix 1: The vicious cycle in the pathogenesis of acute compartment syndrome**

*Trauma and Emergency Surgery*

#### **Author details**

Balaji Zacharia\* and Raj Vignesh Selvaraj Department of Orthopedics, Government Medical College, Kozhikode, Kerala, India

\*Address all correspondence to: balaji.zacharia@gmail.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

#### **References**

[1] Garner MR, Taylor SA, GausdTen E, Lyden JP. Compartment syndrome: diagnosis, management, and unique concerns in the twenty-first century. HSS J. 2014;10(2):143-152. doi:10.1007/ s11420-014-9386-8

[2] R. Volkmann, "Die ischaemischen Muskellähmungen und Kontrakturen," Zentralblatt für Chirurgie, vol. 8, pp. 801-803, 1881.

[3] McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. The Journal of Bone and Joint Surgery British volume. 2000;82- B(2):200-203. doi:10.1302/0301-620x. 82b2.0820200

[4] Stahel PF, Mauser N, Gissel H, Henderson C, Hao J, Mauffrey C. Acute Lower-leg Compartment Syndrome. Orthopedics. 2013;36(8):619-624. doi:10.3928/01477447-20130724-07

[5] Taylor RM, Sullivan MP, Mehta S. Acute compartment syndrome: obtaining diagnosis, providing treatment, and minimizing medicolegal risk. Curr Rev Musculoskelet Med. 2012;5(3):206-213. doi:10.1007/s12178-012-9126-y

[6] Stella M, Santolini E, Sanguineti F, et al. Aetiology of trauma-related acute compartment syndrome of the leg: A systematic review. Injury. 2019;50:S57- S64. doi:10.1016/j.injury.2019.01.047

[7] Hutchinson, M.R., Ireland, M.L. Common Compartment Syndromes in Athletes. Sports Med. 17, 200-208 (1994). https://doi.org/10.2165/00007256- 199417030-00006

[8] Hope MJ, McQueen MM. Acute compartment syndrome in the absence of fracture. J Orthop Trauma. 2004 Apr;18(4):220-4. doi: 10.1097/00005131- 200404000-00005. PMID: 15087965.

[9] Hasnain Raza, Anant Mahapatra, "Acute Compartment Syndrome in

Orthopedics: Causes, Diagnosis, and Management", Advances in Orthopedics, vol. 2015, Article ID 543412, 8 pages, 2015. https://doi.org/10.1155/2015/543412

[10] Pechar J, Lyons MM. Acute Compartment Syndrome of the Lower Leg: A Review. The Journal for Nurse Practitioners. 2016;12(4):265-270. doi:10.1016/j.nurpra.2015.10.013

[11] Frink, M., Hildebrand, F., Krettek, C. et al. Compartment Syndrome of the Lower Leg and Foot. Clin Orthop Relat Res , 940-950 (2010). https://doi. org/10.1007/s11999-009-0891-x

[12] Ronel, Daniel N. M.D.; Mtui, Estomih M.D.; Nolan, William B. III M.D. Forearm Compartment Syndrome: Anatomical Analysis of Surgical Approaches to the Deep Space, Plastic and Reconstructive Surgery: September 1, 2004 - Volume 114 - Issue 3 - p 697-705 doi: 10.1097/01.PRS.0000130967.42426.23

[13] Ling, Marcus Z. X. M.B.B.S.; Kumar, V P. F.R.C.S. Myofascial Compartments of the Hand in Relation to Compartment Syndrome: A Cadaveric Study, Plastic and Reconstructive Surgery: February 2009 - Volume 123 - Issue 2 - p 613-616 doi: 10.1097/PRS.0b013e3181956538

[14] Nadeem RD, Clift BA, Martindale JP, Hadden WA, Ritchie IK. Acute compartment syndrome of the thigh after joint replacement with anticoagulation. The Journal of Bone and Joint Surgery British volume. 1998;80-B(5):866-868. doi:10.1302/0301-620x.80b5.0800866

[15] Elliott KGB, Johnstone AJ. DIAGNOSING ACUTE COMPARTMENT SYNDROME. The Journal of Bone and Joint Surgery British volume. 2003;85-B(5):625-632. doi:10.1302/0301-620x.85b5.14352

[16] Oak NR, Abrams RA. Compartment Syndrome of the Hand. Orthopedic

Clinics of North America. 2016;47(3): 609-616. doi:10.1016/j.ocl.2016.03.006

[17] Olson SA, Glasgow RR. Acute Compartment Syndrome in Lower Extremity Musculoskeletal Trauma. Journal of the American Academy of Orthopaedic Surgeons. 2005;13(7):436- 444. doi:10.5435/00124635-200511000- 00003

[18] T. Tollens, H. Janzing & P. Broos (1998) The Pathophysiology of the Acute Compartment Syndrome, Acta Chirurgica Belgica, 98:4, 171-175, DOI: 10.1080/00015458.1998.12098409

[19] Hargens AR, Romine JS, Sipe JC, Evans KL, Mubarak SJ, Akeson WH. Peripheral nerve-conduction block by high muscle-compartment pressure. The Journal of Bone & Joint Surgery. 1979;61(2):192-200. doi:10.2106/ 00004623-197961020-00006

[20] HUARD J, LI Y, FU FH. MUSCLE INJURIES AND REPAIR. The Journal of Bone and Joint Surgery-American Volume. 2002;84(5):822-832. doi:10.2106/ 00004623-200205000-00022

[21] Griffiths DLl. THE MANAGEMENT OF ACUTE CIRCULATORY FAILURE IN AN INJURED LIMB. The Journal of Bone and Joint Surgery British volume. 1948;30-B(2):280-289. doi:10.1302/ 0301-620x.30b2.280

[22] Cascio BM, Wilckens JH, Ain MC, Toulson C, Frassica FJ. Documentation of Acute Compartment Syndrome at an Academic Health-Care Center. The Journal of Bone & Joint Surgery. 2005; 87(2):346-350. doi:10.2106/jbjs.d.02007

[23] Murdock M, Murdoch MM. Compartment Syndrome: A Review of the Literature. Clinics in Podiatric Medicine and Surgery. 2012;29(2):301- 310. doi:10.1016/j.cpm.2012.02.001

[24] von Keudell AG, Weaver MJ, Appleton PT, et al. Diagnosis and treatment of acute extremity compartment syndrome. The Lancet. 2015;386(10000):1299-1310. doi: 10.1016/s0140-6736(15)00277-9

[25] Pechar J, Lyons MM. Acute Compartment Syndrome of the Lower Leg: A Review. J Nurse Pract. 2016; 12(4):265-270. doi:10.1016/j.nurpra. 2015.10.013

[26] Frink M, Hildebrand F, Krettek C, Brand J, Hankemeier S. Compartment syndrome of the lower leg and foot. Clin Orthop Relat Res. 2010;468(4):940-950. doi:10.1007/s11999-009-0891-x

[27] Mith??fer K, Lhowe DW, Vrahas MS, Altman DT, Altman GT. Clinical Spectrum of Acute Compartment Syndrome of the Thigh and Its Relation to Associated Injuries. Clinical Orthopaedics and Related Research. 2004;425:223-229. doi:10.1097/00003086-200408000- 00032

[28] Nathan ST, Roberts CS, Deliberato D. Lumbar paraspinal compartment syndrome. International Orthopaedics (SICOT). 2012;36(6):1221- 1227. doi:10.1007/s00264-011-1386-4

[29] Botte MJ, Gelberman RH. ACUTE COMPARTMENT SYNDROME OF THE FOREARM. Hand Clinics. 1998;14(3): 391-403. doi:10.1016/s0749-0712(21) 00398-x

[30] Codding JL, Vosbikian MM, Ilyas AM. Acute Compartment Syndrome of the Hand. The Journal of Hand Surgery. 2015;40(6):1213-1216. doi:10.1016/j.jhsa.2015.01.034

[31] McMillan TE, Gardner WT, Schmidt AH, Johnstone AJ. Diagnosing acute compartment syndrome—where have we got to? International Orthopaedics (SICOT). 2019;43(11):2429-2435. doi:10.1007/s00264-019-04386-y

[32] Beniwal RK, Bansal A. Osteofascial compartment pressure measurement in *Acute Compartment Syndrome of the Extremities and Paraspinal Muscles DOI: http://dx.doi.org/10.5772/intechopen.97841*

closed limb injuries – Whitesides' technique revisited. Journal of Clinical Orthopaedics and Trauma. 2016;7(4):225- 228. doi:10.1016/j.jcot.2016.01.001

[33] Bariteau JT, Beutel BG, Kamal R, Hayda R, Born C. The Use of Near-Infrared Spectrometry for the Diagnosis of Lower-extremity Compartment Syndrome. Orthopedics. 2011;34(3):178- 178. doi:10.3928/01477447-20110124-12

[34] McMillan TE, Gardner WT, Schmidt AH, Johnstone AJ. Diagnosing acute compartment syndrome—where have we got to? International Orthopaedics (SICOT). 2019;43(11):2429- 2435. doi:10.1007/s00264-019-04386-y

[35] Osborn, Col. Patrick M. MD; Schmidt, Andrew H. MD Management of Acute Compartment Syndrome, Journal of the American Academy of Orthopaedic Surgeons: February 1, 2020 - Volume 28 - Issue 3 - p e108-e114 doi: 10.5435/JAAOS-D-19-00270

[36] Long B, Koyfman A, Gottlieb M. Evaluation and Management of Acute Compartment Syndrome in the Emergency Department. The Journal of Emergency Medicine. 2019;56(4):386- 397. doi:10.1016/j.jemermed.2018.12.021

[37] Wall CJ, Lynch J, Harris IA, et al. Clinical practice guidelines for the management of acute limb compartment syndrome following trauma. 2010; 80(3):151-156. doi:10.1111/j.1445- 2197.2010.05213.x

[38] Lin JS, Samora JB. Pediatric acute compartment syndrome: a systematic review and meta-analysis. 2020;29(1):90- 96. doi:10.1097/bpb.0000000000000593

[39] Stella M, Santolini E, Sanguineti F, et al. Aetiology of trauma-related acute compartment syndrome of the leg: A systematic review. Injury. 2019;50:S57- S64. doi:10.1016/j.injury.2019.01.047

[40] Konda SR, Kester BS, Fisher N, Behery OA, Crespo AM, Egol KA. Acute Compartment Syndrome of the Leg. 2017;31(3):S17-S18. doi:10.1097/bot. 0000000000000894

[41] Köstler W, Strohm PC, Südkamp NP. Acute compartment syndrome of the limb. Injury. 2005;36(8):992-998. doi:10.1016/j.injury.2005.01.007

[42] Fulkerson E, Razi A, Tejwani N. Review: Acute Compartment Syndrome of the Foot. Foot Ankle Int. 2003;24(2): 180-187. doi:10.1177/10711007030 2400214

[43] Ojike NI, Roberts CS, Giannoudis PV. Compartment syndrome of the thigh: A systematic review. Injury. 2010;41(2):133- 136. doi:10.1016/j.injury.2009.03.016

[44] Alexander W, Low N, Pratt G. Acute lumbar paraspinal compartment syndrome: a systematic review. ANZ J Surg. 2018;88(9):854-859. doi:10.1111/ ans.14342

[45] Kistler JM, Ilyas AM, Thoder JJ. Forearm Compartment Syndrome. Hand Clinics. 2018;34(1):53-60. doi:10.1016/j.hcl.2017.09.006

[46] Rubinstein AJ, Ahmed IH, Vosbikian MM. Hand Compartment Syndrome. Hand Clinics. 2018;34(1): 41-52. doi:10.1016/j.hcl.2017.09.005
