Causes of Rising Intracranial Pressure
Rising Intracranial pressure also called increased intracranial pressure abbreviated as ICP is the gradual or sudden rise in the pressure within the brain. The pressure usually increases because of the rising amount of fluid within the brain. A keen evaluation of the level of blood within the brain shows that sudden tumor rupture or brain injury leads to increased intracranial pressure (Hawthorne, & Piper, 2014). Furthermore, the ICP results from the swelling brain tissues, because of illness or injuries. Such disease can be epilepsy. In case of defining the increased intracranial pressure, Munroe-Kellie hypothesis is very much important. According to this hypothesis, the volume of the cranial compartment is fixe and inside the compartments are filled with the components like blood, brain tissues and fluid and they are responsible for creating an equilibrium condition inside the cranium that is enhancement of volume in any of the components of cranium will cause decrease in volume of the other components to maintain the equilibrium. To maintain this equilibrium in ICP, there is a mechanism called autoregulation and it is a neuroprotective mechanism that regulates the cerebral blood flow into the nerve tissues when there is high blood pressure. When, the cerebral blood flow increases there is a vasoconstriction in the arterioles and when the blood flow is decreased vasodilation occurs to enhance the blood flow in order to continue the oxygen supply to the brain tissues. This mechanism is called autoregulation and helps in maintaining ICP in a normal range (White & Venkatesh, 2016). In summary, brain injuries cause ICP, which leads to brain damage. Therefore, an evaluation of the case studies of Tamara and Leo shows that increased intracranial pressure is a life-threatening condition hence any person showing its signs and symptoms should get an immediate emergency medical attention.
The case tutorial of Tamara and Leo showed the signs and symptoms of rising intracranial pressure. In the case of Tamara, she fell while playing; this must have caused brain injuries specifically subdural haematoma. Thus, the injuries raised pressure within her brain, which led to ICP. On the other hand, Mr. Leo must have experienced inflammation in the nerve tissues in the brain tissues which intern increased pressure within his brain causing raised intracranial pressure. In both cases, the following were the observed vital signs and symptoms of elevated ICP; a headache, optic disc swelling, vomiting, and seizures. These are the significant indicative signs and symptoms of the ICP. Nonetheless, there are general signs and symptoms of raised intracranial pressure, which were poorly described in the case studies. All these signs and symptoms, indicated in the case studies, are also indicators of stroke, recent head injury or brain tumor.
Autoregulation and Its Role in Maintaining Normal Range Intracranial Pressure
There are other signs and symptoms of increased intracranial pressure despite the identified vital signs and symptoms in the case of Tamara and Leo. The combination of a headache, vomiting, optic disc swelling, and seizures are the generally known essential indicators of raised increased intracranial pressure, although records show that there are minimal correlations between the vital signs and symptoms and that of hypertension. Additionally, Fundal haemorrhages gradually develop because of the severe and acute ICP when the patient has experienced subarachnoid haemorrhages like in the case of Mr. Leo or during head injuries like in the case of Tamara (Qureshi, et al., 2016: p.1041). If the elevated ICP persist, it can fail to exhibit the signs and symptoms of optic disc swelling, especially if the subarachnoid sleeves within the optic nerves fail to signal the subarachnoid space (Binenbaum et al., 2013).
Moreover, vomiting is usually the following characteristic of ICP that generally occurs after waking up in the morning and is often identified with the morning headaches. Progressive deterioration in the conscious human level is also a characteristic of ICP. The conscious decline assessed by the Glasgow Coma Scale (GCS), and it is also a consequence of caudal dislodge of midbrain and diencephalon. In general, there are minor indicators of raised intracranial pressure such as bilateral ptosis, papillary dilation, respiratory irregularity, an extension to pain and impaired upgaze. The minor symptoms are usually related to the tonsillar herniation or tentorial beside the absolute increasing intracranial pressure. There are other late signs and symptoms include blood pressure, respiratory patterns, and pulse. These signs are similar to ischemia or brain stem distortions (Alali, et al., 2013: p.1043). In case of Tamara, it is seen that he had a loss of consciousness and vomiting that was the sign of ICP. In addition she also had a bad GCS score that is an assessment tool of consciousness. She had the GCS score with disorientation (best verbal Response 4, best motor response 5, eye opening 4). In case Leo, it was seen that he had severe headache. While assessing the late sign it was found that , he had general symptoms of ICP such as irregularity in breathing, high blood pressure, droopy right eye and downgaze. The right eye droopiness is the symptoms of right third cranial nerve palsy. After primary examination it was found that Tamara had pulse rate of 124, high breathing rate of 28 and those were the late signs of ICP. During checking of late signs in Leo it was found that, he had a GCS score of 12 ( eye opening 3, best motor response 5 and best verbal response 4) and that was a crucial vital sign of elevated ICP.
Signs and Symptoms of Intracranial Pressure: Case Studies of Tamara and Leo
Pathophysiology of a headache: A headache due to the elevated intracranial pressure can cause various other physiological problems such as excessive cerebrospinal fluid around the brain, the tumour of the brain, swellings, and bleeding in the brain. The brain is insensitive to pain since it does not have pain receptors (Andrews, et al., 2015: p. 2404). However, there are parts within the skull and the neck endowed with pain receptors such as venous sinus, middle meningeal artery, spinal and cranial nerves, extracranial arteries, eyes, mouth linings, teeth, and ears. A headache caused by irritations or traction of the blood vessels and meninges. In case of Leo it was seen that, he had symptoms like headache, meningitis and severe photophobia and Leo was suspected to have a subarachnoid haemorrhage Hunt Hess Grade III. Additionally, in the case of nociceptors stimulations by head tumour or trauma, a person can experience headaches. The blood vessel spasms, dilation of blood vessels, infection of meninges, inflammations and muscular tensions may lead to nociceptors stimulations, which intern causes pain. Upon stimulation, the nociceptors signal to nerve fibers to the nerve cells located in the brain that there is part of the body that is experiencing hurts (Mitsi & Zachariou, 2016). The ICP headaches are deduced to be bursting or throbbing, and they generally worsened by accelerating factors of increased intracranial pressure like recumbency, sneezing, coughing or exertion. Notably, the raised intracranial pressure is worse in the morning than any other time; this is due to the ICP during the night as a result of recumbency, increased CSF absorption and increased PCO2 when one is asleep as result of respiratory depressions.
Nonetheless, the intracranial pressures exhibit tensional headaches. The tensioned headaches of ICP follow the same physiology through stimulation of the peripheral neurons in the neck and head muscles. Clustered headache is also a sign of ICP that involves the over-activation of the hypothalamus and the trigeminal nerves.
Vomiting pathophysiology: when the receptors, located below the ventricles of the brain prompts chemoreceptor site called area postrema, there is stimulation of vomiting. The postrema is described as a circumventricular combination of tissues and located out of the blood-brain barriers (Maekawa, et al., 2015: p. 426). The vomiting centre is situated in the central medulla and the projections from this sections firstly connects to the spinal motor neurons and vagus nerves that ultimately innervate the abdominal smooth muscles. In the area of postrema, the chemoreceptor trigger zone (CTZ) is located and it is directly associated with the vomiting. In the vomiting centre muscarinic and histamine receptors are present and the in the CTZ region, histamine receptors (5HT-3) and dopamine (D2) recptors are present. The receptor 5HT-3 has a direct peripheral effect on the gastrointestinal tract. Along with this, afferent input is sent to the vomiting centres by the sensory vestibular systems and limbic cortex (Bhakta & Goel 2017). The vestibular system signals the brain through cranial nerve VIII, which in turn plays a pivotal role in motion illness as well as being rich in histamine H 1 receptor and muscarinic receptors. The vagus nerve or cranial nerve stimulated in case of pharynx irritation, leads to the gag reflex (Wiesmann, et al., 2015: p.1075). Hence, the enteric neuron and vagal nerve signal the brain in regards to the gastrointestinal system leading to vomiting. On the other hand, CNS intervenes on the stress emanating from the higher brain and psychiatric disorders.
Pathophysiology of Headaches Due to Elevated Intracranial Pressure
Papilloedema pathophysiology: It is characterized by blurred vision in both eyes or in some cases lost vision for a few seconds. It also attracts headaches and vomiting. On the other hand, optic disc is a vital sign of raised intracranial pressure, though it takes time for the raised pressure to develop fully. The swelling due to the local inflammation of the optical disc, is the result of axoplasmic flow stasis along with the intra-axonal edema in optic disc region. The optic nerve sheath is continued up to the subarachnoid space of the brain. As a result increase in the pressure of cerebro spinal fluid (CSF) can also able to enhance the pressure in the optic nerve and the optic nerve then can act as tourniquet to obstruct the axoplasmic transport. This may cause alteration in the level of lamina cribosa and as a result, swelling of the nerve head occurs. Hence, the pressure becomes asymmetrical, which leads to protrusion and pinch of the neuron’s head. The fibers within the retinal ganglion cells located at the optic disc tend to be turgid, hence bulging anteriorly. The constant and extensive optic neuron’s head swells, or the optic disc edema leads to lost fibers or even permanent impaired vision (Ljubisavljevi? & Trajkovi?, 2016).
Seizures: Sign and symptom of vital raised intracranial pressure include seizures. The pathophysiology of seizures is as follows. Seizures result from paroxysmal discharges from a combination of specific neurons, which emanates from abnormal loss or excitation of inhibition. Synapse is the central unit of neurotransmitters. Additionally, the ion channels are the fundamental constituents of synapses (Crossley, et al., 2014: p.75). Hence, the cause of the seizures can be narrowed down to malfunctioning of the pathways of ions. Close to a third of the seizures are as a result of genetic abnormalities of ion channels while a quarter results from structural lesions. Hence, patients who show signs of lesions commonly exhibit neurological abnormalities (Adelson, et al., 2013: p.552). There are environmentally acquired lesions such as infections, traumatic brain injuries, perinatal brain, and brain tumour.
On the other hand, there are lesions which either have strong genetic components or are genetically caused such as brain malformations, metabolic disorders, and genetic tumor syndromes. In the case of half seizures disorders, absolutely no structural or genetic abnormalities exhibited. Therefore, several causes are either acquired or genetic. The cause of seizures in Tamara was not genetic as she did not have any past history of seizures in her family. So it can be said that, Tamara had her seizure because of the fall she had during the play. She had seizures as she had parietal hematoma on her scalp that might cause seizure in Tamara. In case of Leo, he had headache during his work and there was no fall related cases. So it might be happen that, Leo’s seizures may be genetically inherited. Leo had a sudden headache during his work and it was a sign of elevated ICP. The elevated ICP is associated with seizures and there migt be rebleed in the subarachnoid haemorrhage and assessment of Leo indicated towards the fact that he might have subarachnoid haemorrhage. Besides the environmental and genes influences, the brain synapse growth has a robust effect on the seizures. The seizure is dynamic and thus explaining why most seizures commence then halts for no apparent reason when a child grows. Based on the seizures dynamics, the seizures are categorized into different epileptic syndromes, partial or focal and tonic-clonic.
Pathophysiology of Vomiting and Papilloedema in Intracranial Pressure
The family plays a pivotal role in recognizing the signs and symptoms of intracranial pressure as well as improving the care of patients diagnosed with ICP. Importantly, in both tutorial case studies of ICP, the families ensured that the standard 8 of National Safety and Quality Healthcare Services (NSQHS) developed by Australian Commission on Safety and Quality in Healthcare were adhered to, diligently. According to the NSQHS, the public is protected from harm and also entitled to better healthcare service provisions (Rickard, et al., 2013: p.681). The standard 8 of the NSQHS which suggests that the families should recognize and respond to the clinical deterioration of the patients was adhered to by the family of Tamara and Mr. Leo.
The standard nine guidelines suggest: establishing response and recognition- The families of Leo and Tamara ensured that the national consensus statement between them and the clinician was used to enhance the support and promoting recognition and response when their patients’ conditions were deteriorating at the emergency and during the period of admissions (Song et al., 2015: p.90). Secondly, the families are expected to recognize the clinical deterioration and escalation of care. When Tamara’s head was swelling, the family recognized and informed the clinicians. On the other hand, when Leo was subconscious, the family alarmed the clinicians for appropriate action. Thirdly, the NSQHS suggests that the family should respond to the clinical deterioration (Campling et al., 2018). In this scenario, patients’ family is very much important as they can observe the patients and as a result they have the best opportunity to report about the condition of the patient. This will ultimately help in recognizing the patients’ symptoms as early as possible (Roland, 2015). Lastly, the families are to communicate with the patients and caregivers at any time to get the progress of the patients to escalate the patient’s care (Brady et al., 2015 p.200). In general, Tamara’s family echoed the headaches, irresponsive to stimuli, breathing difficulties and other dangers, which the clinicians responded promptly because her health was deteriorating. On the other hand, the family of Leo, responded to the dangers, irregular breathing, irresponsive to certain stimuli and other subarachnoid hemorrhages characteristics by informing the clinicians to escalate the Leo’ deteriorating condition.
In summary, both case studies showed the signs and symptoms of raised intracranial pressure. The causes of ICP, exhibited in the case study of Tamara and Leo were similar though there were certain exceptions. The ICP resulted from brain injuries when Tamara was playing while Leo’s ICP condition arose at work, which could have led from genetic influence. Among the similar signs and symptoms portrayed by the two include a headache, vomiting and Papilloedema and seizures. Additionally, according to standard 9 of National Safety and Quality Healthcare Services (NSQHS), the family should play a vital role in ensuring that the care of patients is recognized and escalated.
Seizures as a Sign and Symptom of Vital Raised Intracranial Pressure
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