The patient in the case study is an old managed 62 years old who had collapsed at the shopping center after feeling extremely dizzy. The patient is awake, sitting down but is disoriented and drowsy. Even though he has difficulty in talking, he can remember what happened before he fell. The information from her daughter indicates that eight months ago, he also had a falling episode from the stairs but did not sustain any major injury. Suddenly, his eyes move upwards and he began to experience seizures. The paper will discuss the key clinical signs from the provided case, provide differential diagnoses, and the underlying rationales. Furthermore, it will discuss the pathophysiology of the diagnosis and its management practices. Finally, the paper will critique the presented evidence that supports the management practices before concluding
Primary signs and symptoms for the case
From the case study, the following primary signs and symptoms were observed from the patent
- Difficulty in talking (slurred speech)
- No memory loss
- Collapsed after feeling extremely dizzy
- Eye dilation
- Had a falling episode 8 months ago
Differential Diagnosis One: Benzodiazepine Abuse
Benzodiazepines affect the major brain neurotransmitters called gamma-aminobutyric acid (GABA). According to Baldwin (2013, pp. 967-71), this neurotransmitter on motor neurons has an inhibitory effect, hence the GABA presence stops or slows the activity of the neurons. Benzodiazepines enhance the GABA activity, slowing nerve impulses effectively throughout the body. The nervous systems of the human body have two different types of the receptor of Benzodiazepines. One eliciting the sedative effect, and one causing the anti-anxiety effect (Buisman-Pijlman 2009, pp.210-211).
Despite pharmacological mechanisms that underlie Benzodiazepines withdrawal and tolerance are complex. According to Ashton (2005, pp.249-255), tolerance to chronic administration of Benzodiazepines results from the neuro-adaptive process that involves both desensitizations of the inhibitory receptors of γ-aminobutyric acid (GABA) and sensitization of glutaminergic receptors that are excitatory. Both of these systems according to Ashton (2005, pp.249-255) involves multiple receptor subtypes
GABA receptors changes may include conformational alterations towards a state of low affinity for GABA and also uncoupling of the receptors of Benzodiazepines from their sites on some GABA receptors. This is followed by internalization and sometimes long term effects of intraneural transcription of genes. On the other hand, glutaminergic system changes may include N-methyl-D-aspartate (NMDA) sensitization and possibly also other receptors.
Ashton (2005, pp.249-255) pointed out that Abrupt or rapid Benzodiazepines withdrawal once tolerance has been developed predisposes the recipient to all of these drug-induced adaptations consequences. This results in the under activity of the inhibitor functions of GABA and a surge in the excitatory activity of the nerves, resulting in many of the withdrawal symptoms of Benzodiazepines such as confusion, drowsiness, dizziness, blurred vision, slurred speech, weakness, difficulty in breathing, lack of coordination, coma, insomnia, anxiety, seizures and autonomic hyperactivity (Jermaine 2012, pp.8; Rosario and Hidalgo (2015, pp 13).
Paramedic Intervention and Rationale
- Pre-hospital management of Benzodiazepines abuse
Just like any other overdose case, the first step is to ado an assessment of the patient’s airway, circulation, and breathing and if needed, rapidly address them. The cornerstone of Benzodiazepines overdoses treatment is good monitoring d supportive care. The pre-hospital care for the patient who is suspected to have overdosed benzodiazepines includes the following; airway support and supplemental oxygen, intravenous (IV) access, cardiac monitoring, and also the rapid determination of glucose (finger stick) and if necessary administration of D50 (Lehne 2007).
Lehne (2007) pointed out that a single dose of activated charcoal in most instances is not recommended because the risks superseded the benefits. Benzodiazepines overdoses are rarely fatal but aspiration risks from oral charcoal dose can greatly increase the altered mental status
Lehne (2007) indicated that Naloxone can also be administered to the patient at a very low dose of 0.05mg and increasing it gradually if there is a need if opiate co-ingestion is also suspected or the diagnosis is unclear. For instance, if the patient is having severe respiratory depression. However, Lehne (2007) cautions that although naloxone in low dosage will reverse respiratory depression in opioid overdose patients, it can cause severe withdrawal symptoms like vomiting and nausea to the opioid-dependent. This can lead to aspirations of the patient’s gastric contents who are unable to protect their airway because of Benzodiazepines sedation.
Similarly, Lehne (2007) asserted that the use of Flumazenil in acute Benzodiazepine overdose is still controversial as much as it is the only antidote. Its risks also outweigh the possible benefits. In long term users of Benzodiazepines, flumazenil may precipitate seizures and withdrawal. Similarly, for the patients taking Benzodiazepines as a medication, flumazenil may exuberate the conditions
- Future Intervention for Benzodiazepines abuse
After the delivery of the patient to the hospital, several long-term management interventions will be administered. Upon arrival at the hospital, the diagnosis will be done to the patient based on his medical history, lab tests, and examination. For acute ingestions, diagnosis can be easy since the family members will tell the doctor what the patient took. However, for the chronic drug abuser, it might be difficult to diagnose especially if the patient or the family tries to cover up.
The workup of the emergency departments for any possible overdose of toxic drugs consists of initial evaluation (Jermaine 2012, pp.8). The doctors will assess how well the patient is breathing. Moreover, monitoring and testing will take place in the emergency department where the patient will place on a monitor that evaluates pulse oximetry, blood pressure, and heart rate. An IV line will also be inserted and if the patient has a reduced conscious level or have shortness of breath, oxygen will be given. Jermaine 2012, pp.8), stated that sometimes urine drug screens are performed. All these lab tests are done to detect most of the drugs commonly abused including benzodiazepines. Chest X rays, ECGs, and blood samples can also be obtained if the doctors have a concern that the patient may have ingested dangerous drugs.
For the medical treatment for acute toxicity of benzodiazepines abuse, it normally depends on how much the patient took. If the drug was taken by the patent in the last 1-2 hours, gastric lavage may be considered by the doctor. With its procedure, Jermaine (2012, pp.8) elaborated that a large tube is inserted through the mouth into the patient’s stomach. Large volumes of water are then directed into the stomach to wash the fragments of the pill. However, this procedure is not often used and can be applied only if the patent is known to have ingested other medications that are potentially lethal
Similarly, the activated charcoal in a single dosage is also recommended for the patients who were brought within 4 hours after drug ingestion. This prevents medication absorption. However, it has other side effects such as abdominal cramps, vomiting, and nausea. However, the only antidote for countering benzodiazepines toxic effects known as Flumazenil or Romazicon reverses benzodiazepines’ sedative effects. However, it can cause seizures and withdrawals for chronic benzodiazepines abusers patients.
Lastly, for the chronic abusers, treatment can be done at home or rehabilitation centers with the help of a doctor. The initial step is the reduction of benzodiazepines gradually to prevent seizures and withdrawal. This is a better option compared to the prolonged recovery phase where the patent tries to stay free of drugs. Social support from friends and family is also helpful to the patient.
Differential Diagnosis Two: Subdural Hematoma (SDH) Due To Previous Fall
According to Adhiyaman et al (2002), the usual pathophysiological mechanisms that result in the acute subdural hematoma is a great impact on the skull of a human being. This causes the tissues of the brain to decelerate and accelerate relative to the dural structures that are fixed, hence tearing the blood vessels. The torn blood vessel in most instances is a vein connecting the brain’s cortical surface to a dural sinus (referred to as bridging vein). Jolobe (2002) indicated that in elderly persons, because of brain atrophy, these bridging veins may be already stretched.
Alternatively, Munro & Merritt (1936) stated that a cortical vessel, either a small artery or a vein can be damaged by laceration or a direct injury. An acute subdural hematoma that resulted from a ruptured cortical artery may be linked with only minor head injury, possibly without an associated contusion of the cerebral area. In a study done by Yadav et al (2011, pp. 45-47), the study found ruptured cortical arteries to be situated around the Sylvian fissure
Low-pressure venous bleeding, typically from the bridging veins away from the dura dissects the arachnoid. This blood layers out from the bleeding veins along the cerebral convexity. Zanini et al (2007pp. 68-72) indicated that cerebral injury comes as a result of associated intraparenchymal insults, increased intracranial pressure (ICP), and direct pressure. The clotted blood in the sub-acute phase liquefies. However, the cellular elements in the chronic phase, have already disintegrated, and a serous fluid collection remains in the subdural phases. Moreover, in most rare cases, there is a development of calcification.
Tanaka & Ohno (2013, pp. 55-61) asserted that the main brain injury linked with subdural hematoma plays a significant role in the mortality of patients. However, it is thought that most subdural hematomas result from the torn bridging veins, as evidenced by autopsy or surgery. Besides, not all subdural hematomas are not related to a diffuse injury of the parenchyma. As discussed earlier, most patients sustaining these lesions have the ability to speak before the deterioration of their conditions. However, this is an unlikely scenario for patients who have sustained diffuse damage.
Mallory and Herriott (2015, pp.1-11) demonstrated using a primate model that the rate of heads acceleration-deceleration was the major determinant in the failure of the bridging vein. By using an apparatus that controlled the movement of the head and minimized contact or impact phenomena, they were able to produce in rhesus monkeys acute subdural hematomas. The sagittal head movement in all cases produced an angular acceleration that resulted in overlying subdural hematoma from the rupture of the parasagittal bridging veins. The results from the study done by Mallory and Herriott (2015, pp.1-11) was consistent with the subdural hematomas clinical causes, in that 72% are linked to assaults and falls, and only 24% are related to vehicular trauma. The rates of acceleration or deceleration caused by assaults and falls are greater compared to those caused by mechanisms of energy-absorbing in cars such as deformable steering wheels, dashboard padding, and laminated windshields (Mallory and Herriott 2015, pp.1-11).
Similarly, Honda et al (2015, pp. 985-92) indicated that chronic subdural hematoma is associated commonly with cerebral atrophy. It is thought that cortical bridging veins to be under high tension as the brain shrinks gradually from the skull. Minor trauma can cause one of these veins to rupture. The slow rate of bleeding from the venous system of low pressure often results in the formation of large hematomas before the appearance of clinical signs
According to Richard, Wu & Lin (2015, pp. 12-22), small subdural hematomas spontaneously resorb often. However, larger subdural blood collection normally organizes forming vascular membranes encapsulating the subdural hematoma. Repeated episodes of bleeding from the friable, small vessels within these membranes may explain the expansion of some of the chronic subdural hematomas. Similarly, liquefaction of an acute subdural hematoma may result in the evolution of chronic subdural hematoma. This usually occurs after one to three weeks. Moreover, Matsuyama et al (1997, pp. 193-7) elaborated that some chronic subdural hematomas may occur as a result of enlargement of an osmotic gradient, that draws more fluid into the subdural space, or through another different mechanism referred to as calcification.
As the expansion of the subdural hematoma occurs in the subdural space, it raises the increased intracranial pressure (ICP) and deforms the brain. Initially, the rise in intracranial pressure is compensated by cerebrospinal fluid (CSF) efflux towards the axis of the spine and the venous system compression, expediting drainage of the venous through the jugular veins Adhiyaman et al (2002). At this stage, Jolobe (2002) stated that intracranial pressure rises relatively slowly since the intracranial compliance is high relatively. In summary, the initial intracranial volume changes are associated with small changes in the intracranial pressure.
However, as the hematoma expands, it reaches a limit beyond if it passes, there is a failure in the compensatory mechanisms. The intracranial compliance starts to reduce as a result of small intracranial volume increases that are linked to larger ICP increases. The intracranial pressure exponentially rises, leading to cerebral perfusion that is decreased and global cerebral ischemia. In a hematoma that is expanding rapidly, the entire process can occur in minutes (Munro & Merritt, 1936).
In subdural hematoma patients, bleeding from the bridging veins may result in certain clinical symptoms that have slower onset because the veins have lower pressure compared to the arteries. These signs and symptoms may include a combination of the following; a history of head injury recently, fluctuating levels of consciousness or loss of consciousness, seizures, irritability, numbness, pain, dizziness, headache, amnesia, disorientation, lethargy or weakness, loss of appetite, vomiting or nausea, slurred speech, personality changes, altered patterns of breathing, loss of muscle control, blurred vision, hearing ringing or hearing and lastly abnormal eye movements or deviated gaze.
Paramedic Intervention and Rationale
- Pre-hospital management of Subdural Hematoma (SDH)
This phase marks the beginning of the secondary cerebral injury, where the therapy’s primary goals are treatment and avoidance of hypoxia and hypotension, which are linked with worse clinical results. The priority should be managing the ABCs. The airway of the patient should be managed, ranging from endotracheal intubation observation. Hypotension correction is achieved with isotonic crystalloid through intravenous fluid resuscitation. Myburgh et al (2007) indicated that resuscitation with albumin has been linked to harm, and there has not been any demonstration of benefits with hypertonic saline resuscitation. For the patients with GCS of ≤ 8, endotracheal intubation is generally considered in the field. However, its benefits compared to the bag-mask is still debatable. Moreover, care should be taken by the paramedics to stabilize the cervical spine while the patient is transported to the hospital rapidly. While maintaining immobilization, the basic life support procedures are accepted such as chin-tilt/head tilt or jaw thrusts (Digna and Kool 2007, pp.135).
According to Digna and Kool (2007, pp.135), prehospital endotracheal intubation, as well as nasotracheal intubation and the rapid sequence in a scene of a suspected cerebral hemorrhage, has been extensively debated in the medical literature. Recent medical literature supports the argument that extending scene times significantly in managing the airway is not beneficial and may lead to worse outcomes. For instance, in all trauma situations, Lockey (2001, pp.5-15) indicated that all healthcare providers need to be mindful and minimize scene times and make consideration of performing the procedures necessary on their way to the hospital
Assessment and management of the respiratory rate and effort of the patent should be done as needed. If a patient is suspected of cerebral hemorrhage or subdural hematoma, the medic should administer supplemental oxygen, to avoid anoxia or hypoxia. The recommended oxygen saturation to be achieved should be greater than 90% (Mackenzie 2004, pp.70-74).
Digna and Kool (2007, pp.135) pointed out that manually hyperventilating a suspected patent having a subdural hematoma or cerebral hemorrhage is a subject of great debate. It has been argued for a long time that hyperventilation induces hypocapnia, and this results in cerebral vasoconstriction, which may lead to a reduction in cerebral blood flow and reduce the increased intracranial pressure. However, contemporary medical researches questions this practice’s efficacy since hyperventilation can lead to cerebral blood vessels over construction, which may decrease intracranial blood flow significantly and lead to worse outcomes (Lockey 2001, pp.5-15). It is suggested that hyperventilation should only be used for certain clinical signs. For instance, suspected cerebral herniation that is characterized by a fixed and posturing dilated pupil may be an indication that hyperventilation should be used. In such scenarios, adequate inflation of the lungs and hypoventilation prevention is recommended (Honda et al 2015, pp. 985-92).
Several factors will also come into play when medications are administered. For instance, dextrose will be administered if hypoglycemia is present. Anti-convulsion medications may be used in treating seizures, especially benzodiazepines. If increased intracranial pressure is suspected Lidocaine should be considered when endotracheal intubations to be performed (Mackenzie 2004, pp.70-74).
Intravenous access should be established to serve as a route for fluid administration or medication depending on the overall condition of the patient. In situations of a possible subdural hematoma or cerebral hemorrhage, Revell, Porter, and Greaves (2002, pp.494-498) suggested that hypotension should be avoided since it can influence the outcome of the patient negatively. There are several discussion sins regarding the amount and use of intravenous fluids when a subdural hematoma or cerebral hemorrhage may exist. The options of fluid range from boluses of normal saline to a hypertonic solution. As a general rule, Norri-Sederholm (2014) indicated that intravenous access should beget, and infusion of fluid kept to a minimum for the patients at risk of intracerebral hemorrhage.
- Future Intervention for Subdural Hematoma (SDH)
At the hospital at the emergency department, adequate blood pressure (systolic blood pressure > 90 mmHg) and oxygenation (PaO2 > 60mmHg) should be maintained. Vital signs should be monitored, and adjustments to therapy performed for maintenance of cardiopulmonary homeostasis. Furthermore, the neurological assessments should include an initial followed by serial Glasgow Coma Scale (GCS) score determinants (Kyeong-Seok 2011, pp. 512). Intracranial hypertension signs such as decreased responsiveness of the papillary to light, posturing, hypertension with bradycardia, or even abnormalities in respiration should prompt head of bed elevation empiric treatment, osmolar agent (hypertonic saline or mannitol), and hyperventilation. Laboratory assessments include electrolytes, complete blood count, coagulation profile, glucose, urine toxicology, and blood alcohol level. Abnormalities in coagulation should be corrected rapidly. Imaging should also be performed to help in defining the extent of the injury and in guiding subsequent management (Kyeong-Seok 2011, pp.512).
The paper was based on a case scenario of an elderly patient who collapsed in a town center after feeling dizzy. From the primary signs and symptoms, the patient was drowsy, disoriented, had slurred speech, eye dilation, had o memory loss, seizures, and 8 months ago had a falling episode. Based on the symptoms, the paper came up with two differential diagnoses; benzodiazepine abuse and subdural hematoma. Benzodiazepines affect the major brain neurotransmitters called gamma-aminobutyric acid (GABA) through complex pathophysiological processes. This results in many of the withdrawal symptoms of Benzodiazepines such as confusion, drowsiness, dizziness, blurred vision, slurred speech, weakness, difficulty in breathing, lack of coordination, coma, insomnia, anxiety, seizures, and autonomic hyperactivity. On the other hand, the pathophysiological mechanisms that result in the acute subdural hematoma is a great impact on the skull of a human being. This causes the tissues of the brain to decelerate and accelerate relative to the dural structures that are fixed, hence tearing the blood vessels (bridging veins). bleeding from the bridging veins may result in certain clinical symptoms that include a combination of the following; a history of head injury recently, fluctuating levels of consciousness or loss of consciousness, seizures, irritability, numbness, pain, dizziness, headache, amnesia, disorientation among others. Pre-hospital management of both benzodiazepine abuse and subdural hematoma should first begin by managing the ABCs. The airway of the patient should be managed, ranging from endotracheal intubation observation. Further treatment and monitoring should be done when the patient has been admitted to the hospital
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