diff --git a/docs/index/dai-case-report.md b/docs/index/dai-case-report.md new file mode 100644 index 0000000..bf52091 --- /dev/null +++ b/docs/index/dai-case-report.md @@ -0,0 +1,184 @@ +# “Traumatic Brain Damage” +### Diffuse Axonal Injury - by Pavly G. + +## Keywords: +Diffuse Axonal Injury - Traumatic brain injury (TBI) - Motor Vehicle Accident (MVA) - Decerebrate posturing - Brainstem damage + +## Abstract: +Diffuse axonal injury (DAI) is an extensive brain damage as a result of applying sudden shearing forces on the brain tissue usually from successive acceleration-deceleration forces as a consequence of motor vehicle accidents (MVA). The sudden deceleration and the abrupt changes in the angular momentum lead to the application of stretching vectors that stretch out the axons at the gray-white matter interfaces, the higher the deceleration forces, the more severe the axonal stretching vectors. This patient was brought to the ED in a deep coma for intensive care unit admission as a part of the transfer process from another hospital. Ventilatory and hemodynamic support measures were commenced thereafter. An admission emergent spiral NECT full body scan was then commenced before transferring the patient to the intensive care unit. The target of this report is to guide the reader in recognition and life support of such a case, as well as discuss some objective theoretical data that aid the diagnosis of the diffuse axonal injury in the context of traumatic brain injury. + +## Introduction: +Trauma is the most common cause of death in young people, and head injury accounts for almost half of these trauma-related deaths. The severity of the head injury ranges from concussion to severe traumatic brain injury (TBI). The term concussion is broadly defined as an alteration in mental status caused by trauma with or without loss of consciousness, and is often used synonymously with mild traumatic brain injury (mTBI). Grades of traumatic brain injury are defined by the Glasgow Coma Scale (GCS) measured 30 minutes after the injury [1]. Decerebrate posturing, also known as the extensor posture develops if a brainstem transection takes place at or below the level of the red nucleus. This also coincides with the level between the superior and the inferior colliculi within the midbrain which corresponds to the rubrospinal tract origin or its pathway to relay into the ventral spinal horn [3]. The rubrospinal tract carries cortical stimulatory signals to modulate the contralateral anti-gravity or flexor muscle tone effect [3]. On the contrary, the vestibulospinal tract originates from the vestibular nucleus at the pons sending ipsilateral stimulatory reticular fibers to the extensor muscles after synapsing in the ventral spinal horn [3]. Transection of the rubrospinal tract leads to dis-inhibition of the extensor muscle tone, and inhibition of the flexor muscles tone leading to the extensor posturing, this phenomenon is known as “Decerebration” that entails disconnection of the cerebral inhibitory effect on the extensor muscles tone leaving the effect of the vestibulospinal tract unopposed. Decerebrate posturing is described as adduction and internal rotation of the shoulder, extension at the elbows with pronation of the forearm, and flexion of the fingers, the lower limbs also show extension and internal rotation at the hip joint, with extension of the knee and planter flexion of the feet, and toes are typically abducted and hyperextended [2]. There are two reticulospinal tracts on each side of the body, the medial longitudinal fasciculus (MLF) or the medial vestibulospinal tract which originates from the medial vestibular nucleus and terminates in the cervical and upper thoracic levels coordinating head, neck, and eye movements, and the lateral vestibulospinal tract (Deiters’ tract) originating from the lateral vestibular nucleus and terminating with ipsilateral synapses in the ventral spinal horn cells with alpha and gamma motor neurons that then travel to the respective extensor muscles [2, 3]. + +## Case Presentation: +This 37-year-old male patient was brought to the ED for ICU admission as a part of the transfer process from another hospital. The patient was in a deep coma with a GCS of 4/15 at presentation. His relatives had reported that he had had a highway car-collision accident yesterday evening leaving him in a deep coma state. They had transferred him to an ED of another hospital in which he had been intubated, and provided the essential ventilatory and hemodynamic support. The patient’s past medical and surgical history is unremarkable for chronic diseases and recent surgeries or any other concomitant co-morbidity. Familial history is also unremarkable for cardiopulmonary and neurological diseases. Of note, the patient was arrested once in the previous hospital. Unfortunately, the patient died on the fifth day from the admission from a tracheoesophageal fistula, nonetheless, he wouldn’t be likely to survive with this severe traumatic brain injury. + +## Clinical Findings: +General examination showed contusions all over the collision sites, otherwise was unremarkable for ribs and major orthopedic fractures due to collision. Of notice, the patient was arrested once at the previous hospital, so it seemed that he has unilateral left costochondral junction instabilities. The patient was not opening his eye at any time spontaneously or regardless of the stimulus with no interfering factors, he also gave no audible responses regardless of the stimulus, and he had abnormal upper and lower limb extension posturing on pain stimulus which gives him a Glasgow coma score of 4 out of 15 in the format E1-V1-M2. Sensory examination showed maintenance of the extensor posture rigidity on applying fairly crude touch and pain stimulus regardless of the stimulus position whether peripheral or central stimulus. Motor examination of both limbs showed bilateral brisk hyperreflexia patterns with unilateral left positive sustained ankle myoclonus and bilateral absent plantar flexion reflexes. Head and neck examination was unremarkable for cervical spine and rib fractures. Both pupils were maintained at a constriction position with impaired reaction to light directly and consensually, vestibulo-ocular reflexes lateral conjugate movement was bilaterally absent as the eyes are maintained at the mid-line position, and eyes are clear with no petechial hemorrhages or any peri-orbital hemorrhagic collections. Both carotids are palpable. Pulsations are readily unremarkable for any visible delays or thrills. The cardiopulmonary examination was unremarkable for pulmonary edema and murmurs. Abdominal examination was unremarkable for hypochondrial bruising from direct collision. This was all carried out after doing the full body NECT scan as a part of the trauma survey process, and while doing the rest of the routine diagnostic assessments, including an FBC, a Liver Function Test, a Renal Function Test (U&E), Cardiac Enzymes, a Blood Glucose Test, and a Coagulation Profile. + +## Diagnostic Assessment: +#### Patient’s Physical Examination summary: +* Glasgow Coma Scale: 4 out of 15, in the format E1-V1-M2. +* Head & Neck: bilateral non-reactive fixed constricted pupils - impaired light reflex - impaired corneal reflex - impaired vestibulo-ocular reflexes - contusions at the right side of the face (site of impact). +* GCS-P Score: GCS - PRS = 4 - 2 = 2; where “PRS” stands for Pupils Reactivity Score, in this case both pupils aren’t reactive to both the direct and the consensual light reflexes rendering the score 2 [5]. Together with the age, and the brain CT findings, GCS-P carries a prognostic value, follow-up to the discussion, and the analysis sections to know more. +* Sensory Function Examination: maintenance of the extensor posture rigidity on applying fairly crude touch and pain stimulus. +* Motor Function Examination: bilateral brisk hyperreflexia - unilateral left positive sustained ankle myoclonus - bilateral absent plantar flexion reflexes. +* Cardiopulmonary: no signs of significant lung or heart contusions, except for some minute hemorrhagic secretions on arrival at the ED during the basic ventilatory and hemodynamic support. +* Abdomen & Pelvis: no signs of major orthopedic fractures or direct organ contusions from the impact. +#### Patient’s Vitals: +* Sp-O2: 95%-98% when intubated on the mechanical ventilator. +* HR: 110-140 Bpm. +* Bp: 135/98 mm.Hg recorded on the right brachium in the semi-recumbent position. +#### Imaging: +* Full on-admission NECT body scan was made, findings are recorded in the timeline table. +Laboratory testing: +* Full routine laboratory studies was carried-out after the critical care admission including FBC and inflammatory markers, U&E, liver function testing, coagulation profiling, cardiac enzymes profile, arterial blood gases, ECG which was unremarkable at this point. Follow-up to the timeline for the analysis of these studies. + +## Timeline: +| CT Timeline | Imaging | Image Findings | +|-------------|--------|--------| +| Day of accident | | **Brain Meninges**: increased signal intensity along the falx cereberi and the tentorium cerebelli.
**Cerebral hemispheres**: distorted cerebral sulci and gyri patterns, and multiple diffuse white matter punctate hyperdensities.
**Cerebellar hemispheres**: multiple diffuse punctate hyperdensities, and disrupted gray-white matter interfaces.
**Brainstem**: distorted anatomical features with diffuse punctate hyperdensities.
**Ventricular System**: unremarkable for hemorrhagic collections and effacement, except for poor anatomical landmarks for the quadrigeminal and prepontine cisterns.

**Impression**: *Multiple distributed minute punctate hyperdensities likely subcortical contusions.
*Disrupted cerebral and cerebellar gray-white matter interfaces.
*Distorted brainstem features likely brainstem injury. *Increased signal intensity in the falx cerebri and tentorium cerebelli likely subarachinoid bleeders. | + +| Day of admission (Second day after injury) *Calvaria: right side frontoparietal swelling likely subgaleal hematoma. +*Brain Meninges: unremarkable. +*Cerebral/Cerebellar hemispheres: generalized edema, and disrupted gray-white matter interfaces. +*Brainstem: unremarkable. +*Ventricular System: unremarkable for hemorrhagic collections. Mild effacement of the lateral ventricles likely from the minimal effect of the brain edema. + +# Impression: +*This image depicts disrupted cerebral and cerebellar gray-white matter interfaces with mild generalized edema leading to mild effacement of the lateral ventricles on both sides, otherwise is unremarkable for intracerebral hemorrhagic collections. + + + + +US Timeline Image Findings +Second day from admission day Unremarkable studies +Last day * Hepatic focal lesion at the hepatic segment IV probably hepatic contusions. + +* Biliary mud. + +* Tiny splenic calcifc foci. + +* A rim of fluid in the hepatorenal space. + +Laboratory Timeline Admission Day 2nd Day 3rd Day 4th Day 5th Day +FBC, and Inflammatory markers **CRP = 96 *HB = 13.0 mg/dL +#WBCs = 14.4 +Platelets = 189,000 *HB = 10.6 mg/dL +#WBCs = 12.8 +Platelets = 189,000 *HB = 8.7 mg/dL +WBCs = 8.3 +Platelets = 150,000 **HB = 2.8 mg/dL +WBCs = 6.7 +Platelets = 151,000 +**CRP = 154 +U&E (Renal Function Test) ##Urea = 79 mg/dL +#Creatinine = 1.5 mg/dL +Na+ = 136 meq/L +K+ = 4.8 meq/L #Urea = 52 mg/dL +Creatinine = 0.9 mg/dL +Na+ = 140 meq/L +K+ = 4.4 meq/L Creatinine = 1.1 mg/dL +K+ = 4.65 meq/L +##Ca++ (ionized) = 9.0 mg/dL Creatinine = 0.7 mg/dL +*K+ = 3.2 meq/L Na+ = 140 meq/L +K+ = 3.5 meq/L +Liver Function test ##ALT = 60 +##AST = 74 ##ALT = 53 +##AST = 66 #ALT = 39 +##AST = 59 Albumin = 3.4 +Total bilirubin = 0.5 +Direct bilirubin = 0.1 +Coagulation Profile (PT, PTT, INR) #PT = 18.6 +Platelet Count = 13.0 +#INR = 1.49 +#PTT = 44 #PT = 15.7 +Platelet Count = 13.0 +#INR = 1.24 +PTT = 37.8 +Cardiac Enzymes (CPK) ##CPK = 1579 ##CPK = 1560 ##CPK = 1385 LDH = 279 +Arterial Blood Gases (ABG) pH = 7.44 +pCO2 = 38 mmHg +pO2 = 119 mmHg +Glucose = 110mg/dL +HCO3- = 25.8 mmol/L +Temp. = 37 deg.C +D-dimer ##6219.71 +Out of range identifiers:`*` means below baseline, `#` means above borderline, `**` means critically below baseline, `##` means critically above borderline. + +Therapeutic Interventions: +Therapeutic intervention is supportive in this case aiming at stabilizing the patient through both ventilatory and hemodynamic support in addition to continuous monitoring of the physiologic parameters. Emergency Caring has involved cervical spine precautions, airway maintenance including suctioning and auscultation for pneumothorax and hemothorax and connection of the portable mechanical ventilator, and hemodynamic support. The next site was the radiology department where a spiral NECT full body scan was carried-out before intensive care unit admission. At critical care, the patient’s physiologic parameters were monitored carefully and treated accordingly. A full body examination was made thereafter looking for fractures, concealed and external bleeding sources, and then a full neurological examination was commenced. Hypoxemia was avoided by intubation and mechanical ventilation. Of notice, the patient has been recently intubated at the previous hospital. Arterial Pao2 was maintained at borderline 100 mm.Hg, and Paco2 at baseline 35 mm.Hg and not below to avoid cerebrovascular constriction from hypocapnia, and cerebrovascular dilation from hypercapnia; as both of which worsens the cerebral perfusion either by decreasing the mean arterial pressure and increasing the ICP or increasing the cerebrovascular arterial resistance, respectively. A central venous catheter was inserted to monitor the central venous pressure which gives an indication of proper venous return, and thus proper cardiac output and cerebral perfusion. The central venous pressure was maintained at 7 to 12 cm.H2O. Normothermia was maintained at 37 degree Celsius. Low-dose seizure prophylaxis was commenced initially, and increased incrementally as the patient was having sub-clinical fits in the abnormal extensor posture position. DVT prophylaxis was also commenced after the first day as of a pharmacological prophylactic dosage of LWMH, and lower extremity stockings and compression devices. Broad-spectrum antibiotics were commenced for the possibility of aspiration pneumonia as to aid in prevention of fever. + +Therapeutic Timeline: +Timeline Admission Day 2nd Day 3rd Day 4th Day 5th Day +Oxygenation & Intubation *Suctioning & ventilatory care for the pre-intubated tube. +*Mechanical ventilation to maintain the following parameters: +- PaO2 = 100 mm.Hg +- PaCO2 = 35 mm.Hg +- SPO2 >= 95%. +- RR = 12 Bpm +*Hyperventilation is not recommended, and should be used cautiously as it depletes carbon dioxide leading to cerebral vasoconstriction impairing the CBF worsening the brain condition. *Tracheosophageal fistula with a severe paroxysmal fall in SPO2 to below 60%, upper respiratory tract stridor, and abdominal breathing sounds. +Respiration/PEEP *PEEP provides an added positive supportive pressurization at the end of the expiration phase to maintain the pulmonary inflation avoiding alveolar collapse. +*PEEP provides protection against ARDS (Acute Respiratory Distress Syndrome). +*PEEP adjusted to 14-15 cm.H2O pressurization parameters to prevent the increase in ICP. +Hemodynamic support *Maintenance of the following parameters: +- SBP >= 110 mm.Hg +- Hemoglobin >= 7 g/dL +- pH = 7.35 - 7.45 +- Serum sodium = 135 - 145 mEq/L +Glucose, Thiamine & Neurotonics *Maintenance of the glucose levels between (80-180) mg/dL, by adding 25 gm glucose via 50% dextrose IV solutions. +*Thiamine 100mg should be administered with glucose to avoid Wernicke’s Encephalopathy. +Seizures *An initiative loading dose of Levetriacetam 500mg/100mL Saline 0.82% IV b.d for 15 minutes. +*Carried-out an EEG image. *Maintenance dose of Levetriacetam 1000mg/100mL Saline 0.75% IV o.d for 15 minutes. +*Carried-out an EEG image. *Further increase up-to 1500mg/100mL Saline 0.54% IV o.d for 15 minutes. +Anti-High ICP measures *Maintenance of the ICP pressurization below 20 mm.Hg is recommended to prevent the steep decrease of CPP; as CBF = CPP/CVR, and CPP = MAP - ICP. +Venous Thromboembolism Prophylaxis *Enoxaparin (Clexane) 40 mg o.d subcutaneously, an anti-factor Xa level can be measured to adjust the dose accordingly. +Body Temperature *General measures to keep the patient normothermic (37 deg. Celsius), e.g: Paracetamol IV. +Physical Examination (Coma score & Brainstem status) *GCS = 4/15, E1-V1-M2 +*PRS = 2 (Both pupils aren’t reactive to light). +*GCS-P = GCS - PRS = 2. +*Maintenance of extensor posture on applying external stimulus. +*Hyperreflexia +*Hypertonia +*Loss of brainstem reflexes (light reflexes - oculovestibular reflexes - corneal reflexes) +*Left Sustained ankle myoclonus +*Bilateral absent plantar flexion reflex (absent Babiniski sign). *GCS = 3/15, E1-V1-M1 +*PRS = 2. +*GCS-P = 1. +*Areflexia +*Flaccid Paralysis +CBF: Cerebral blood flow. +CVR: Cerebrovascular resistance. +CPP: Cerebral perfusion pressure. +MAP: Mean Arterial pressure. +PEEP: Positive-end-expiratory pressure. +PRS: Pupillary light reactivity score; 2 if both pupils are non-reactive. +GCS-P: Glasgow coma scale pupils score. + + +Discussion: +The evidence from history, physical examination, signs, and diagnostics are all collectively suggestive of a diffuse axonal injury as a result of traumatic brain injury. The physical theory, that highly ascertains the condition, is the abrupt deceleration forces being applied on an accelerating body, these types of forces can be triggered by sudden flips in the direction of the speed of the body [6]. The fact of having obvious disrupted gray-white matter interfaces supports the evidence that this is likely an axonal injury. The supportive clinical signs can be depicted from the brainstem damage manifested as the decerebrate rigidity, the impaired light reflexes with the damaged oculosympathetic pathway, and the impaired vestibulo-ocular reflexes. In fact, the reticular formation and the reticulospinal tracts are parts of the axons that modulate the peripheral nervous system signals, so they are vulnerable to damage by sudden abrupt deceleration forces, as well. The prognosis of the case is considered bad in general, as the survival rate reaches 27% to 32% with a mortality rate ranging from 55% to 60% [Fig-1.1]. By plugging in the NECT findings, the survival rate decreases to even below 20% [Fig-1.2] [7]. A lesson to take home would be the essential knowledge of the basic neuroscience principles to recognize a case of diffuse axonal injury, and determine its severity and prognosis according to the GCS-P modality and serial GCS measurements, in addition, to recognizing the features of brainstem damage, a part of which (pupils’ light reflexes) is essential to complete the GCS-P score modality to reach an approximate prognosis through knowing the survival rate [7]. Furthermore, the incremental steep decrease in hemoglobin, white blood cells count, and platelets combined with high levels of D-dimer over 3 days is highly suggestive of a sort of active internal concealed bleeding. Liver and renal function tests and the total creatine kinase levels are highly suggestive of the possibility of internal organ injury. Rupture of terminal arterioles and intra-parenchymal damage could lead to internal concealed bleeding that is most likely the cause of the steep incremental decrease in hemoglobin levels. The second abdominal sonography, which was carried out at the last day, was highly assertive evidence for abdominal organs’ contusions and internal concealed bleeding especially in the hepatorenal space, though the abdominal sonography carried out on the second day was clear. + +Thumbnails: + +Fig-1.1 - Prognosis Reclaiming from the GCS-P Score (GCS-PA Charts), a simple graphical tool in +the 3-dimensional vector-space. + + +Fig-1.2 - GCS-PA combined with brain CT findings. + + + +Fig-2 - The red nucleus cortical, spinal and cerebellar connections. + + +Fig-3 - The oculo-sympathetic pathway. + +References: +1.Misch, M. R., & Raukar, N. P. (2020). Sports Medicine Update: Concussion. Emergency medicine clinics of North America, 38(1), 207–222. https://doi.org/10.1016/j.emc.2019.09.010 +2.Knight J, Decker LC. Decerebrate and Decorticate Posturing. [Updated 2023 Jul 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559135/ +3.Whitney E, Alastra AJ. Neuroanatomy, Decerebrate Rigidity. [Updated 2023 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK547687/ +4.Jain S, Iverson LM. Glasgow Coma Scale. [Updated 2023 Jun 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513298/ +5.Brennan, P. M., Murray, G. D., & Teasdale, G. M. (2018). Simplifying the use of prognostic information in traumatic brain injury. Part 1: The GCS-Pupils score: an extended index of clinical severity. Journal of Neurosurgery JNS, 128(6), 1612-1620. https://doi.org/10.3171/2017.12.JNS172780 +6.Barth JT, Freeman JR, Broshek DK, Varney RN. Acceleration-Deceleration Sport-Related Concussion: The Gravity of It All. J Athl Train. 2001 Sep;36(3):253-256. PMID: 12937493; PMCID: PMC155415. +7.Murray, G. D., Brennan, P. M., & Teasdale, G. M. (2018). Simplifying the use of prognostic information in traumatic brain injury. Part 2: Graphical presentation of probabilities. Journal of Neurosurgery JNS, 128(6), 16211634. https://doi.org/10.3171/2017.12.JNS172782