Pathophys behind seizure post head injury

EricJRN, MSN, RN · Jun 14, 2008

The pathophys behind this type of seizure is really pretty poorly understood.

http://www.emedicine.com/neuro/TOPIC318.HTM

As far as an NRB mask, I'd leave it unless the patient showed signs of respiratory failure and needed to be ventilated.

Michelle123 · Jun 14, 2008

Thanks for that. I was thinking along the lines of excitotoxicity.

Neuro on a whole is really fascinating!

Daytonite, BSN, RN · Jun 14, 2008

i've got the pathophysiology from two books. if you read and put the information from both together you pretty much have the whole picture.

pathophysiology: the biologic basis for disease in adults and children, third edition, by kathryn l. mccance and sue e. heuther gives the pathophysiology for a tonic-clonic seizure. i'm just going to copy it right out of the book because i have to read their stuff over 10 times along with a medical dictionary to finally get a light bulb to switch on. i'll just type and let you do the thinking! it is from page 472:

"an

epileptogenic focus

appears to be a group of neurons that evidence a paroxysmal depolarization shift and sudden changes in the usual membrane potential. the plasma membranes of neural cells seem more permeable, making them more easily activated by hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, and certain sleep phases. these neurons are hypersensitive and may even remain in a chronic partially depolarized state.

the firing of involved epileptogenic neurons becomes increasingly greater in frequency and amplitude. when the intensity of the neuronal discharge reaches a threshold point, the discharge spreads to adjacent normal neurons through corticocortical synapses. if uninhibited at this point, the cortical excitation spreads through interhemispheric tracts to the contralateral cortex and through projection pathways to the subcortical areas of the basal ganglia, thalamus and brain stem. the excitation spread to the subcortical, thalamic and brain stem areas corresponds to the

tonic phase

(phase of muscle contraction with increased muscle tone) and is associated with loss of consciousness. autonomic clinical manifestations also may emerge at this point, and apnea may be present for a few seconds. the excitation is further projected downward to the spinal cord neurons through the corticospinal and reticulospinal pathways.

the

clonic phase

(phase of alternating contraction and relaxation of muscles) begins as inhibitory neurons in the cortex, anterior thalamus, and basal ganglia begin to inhibit the cortical excitation. this inhibition causes an interruption in the seizure discharge, producing an intermittent contract-relax pattern of muscle contractions. the intermittent clonic bursts gradually become more and more infrequent until they finally cease. at this point the epileptogenic neurons are exhausted and the neuronal membranes probably are hyperpolarized.

the maintenance of seizure activity demands a 250% increase in adenosine triphosphate (atp). cerebral oxygen consumption is increased by 60%. although cerebral blood flow also increases approximately 250% during seizure activity, available glucose and oxygen are readily depleted. with a severe seizure the brain tissue may require more atp than can be produced by the tissues from the available oxygen and glucose. a deficiency of atp, phosphocreatine, and glucose then occurs, and lactate accumulates in the brain tissues. severe seizures thus may produce secondary hypoxia, acidosis, and lactate accumulation, all of which are imbalances that may result in progressive brain tissue injury and destruction. cellular exhaustion and destruction are consequences of these events."

in later pages, the authors ascribe the seizures of brain injuries to compression as a result of either bleeding or swollen tissues.

pathophysiology: a 2-in-1 reference for nurses by springhouse, springhouse publishing company staff has this to say about seizure disorder (pages 330-331):

"seizure disorder, or

epilepsy

, is a condition of the brain characterized by susceptibility to recurrent seizures (paroxysmal events associated with abnormal electrical discharges of neurons in the brain). primary seizure disorder or epilepsy is idiopathic without apparent structural changes in the brain. secondary epilepsy, characterized by structural changes or metabolic alterations of the neuronal membranes, causes increased automaticity.

causes

about 50% of all seizure disorder cases are idiopathic; possible causes of other cases include birth trauma (inadequate oxygen supply to the brain, blood incompatibility, or hemorrhage); perinatal infection; anoxia; infectious diseases (meningitis, encephalitis, or brain abscess); ingestion of toxins (mercury, lead, or carbon monoxide); brain tumors; inherited disorders or degenerative disease, such as phenylketonuria or tuberous sclerosis; head injury or trauma; metabolic disorders, such as hypoglycemia and hypoparathyroidism; and stroke (hemorrhage, thrombosis, or embolism).

pathophysiology

some neurons in the brain may depolarize easily or be hyperexcitable; this epileptogenic focus fires more readily than normal when stimulated. in these neurons, the membrane potential at rest is less negative or inhibitory connections are missing, possibly because of decreased gamma-aminobutyric acid activity or localized shifts in electrolytes.

on stimulation, the epileptogenic focus fires and spreads electric current to surrounding cells. these cells fire in turn and the impulse cascades to one side of the brain (a partial seizure), both sides of the brain (a generalized seizure), or cortical, subcortical, and brain stem areas.

the brain's metabolic demand for oxygen increases dramatically during a seizure. if this demand isn't met, hypoxia and brain damage ensue. firing of inhibitory neurons causes the excitatory neurons to slow their firing and eventually stop. if this inhibitory action doesn't occur, the result is status epilepticus: one seizure occurring right after another and another; without treatment the anoxia is fatal."

you asked, also, in relation to someone that experiences this while they have a non-rebreather mask, (and this will probably be a silly question) is it best to leave it on? or remove it??

i'd leave it on but watch closely to make sure it is staying in place and the patient is not injuring himself. i worked on a neuro unit and even though the siderails were padded, we always had someone standing by the patient's head to protect it if we were there during a seizure since they were thrashing about so violently. you always want to get supplemental oxygen on the patient asap. note, however, that in the early moments of the seizure, the patient may not be breathing. as the seizure subsides, however, you want to check for respiration and be prepared to not only get supplemental oxygen going, but to start rescue breathing.

Michelle123 · Jun 14, 2008

Thanks!

Yeah I see what you mean about having to read it a few times! :)

I'm wanting to get myself a pathophys book, the top one that you mentioned, would you recommend it?

Daytonite, BSN, RN · Jun 15, 2008

i have both books. it depends on how in depth you want to go. the mccance and heuther book is quite large, physically, with over 1600 pages and covers just about everything. i can't pick it up with one hand. it is required for most bsn and master's level classes, i do believe. it is straight pathophys and includes just as i copied it with signs and symptoms (clinical manifestations) and evaluation and treatment for most of the diseases it does address. it has no specific nursing interventions although some might be mentioned. it has charts and illustrations. as i said, i sometimes have to read things over a few times to understand them. when i was answering someone's question on the pathophysiology of the inflammatory response it took me about 4 hours of reading through various paragraphs before i finally "got it" all straight so that i could come up with a nice analogy for it. but, then again, inflammation and allergy response is complicated anyway. there is a newer edition out now and the cost is around $90+.

pathophysiology: a 2-in-1 reference for nurses was written for students. it is organized by body systems and covers the major diseases within each body system. for each there is a description of the disease, causes, the pathophysiology that, i think, is a little easier to read and understand with notes off to the margin titled "how it happens", signs and symptoms, complications, diagnosis (tests done to determine the disease), treatment and nursing considerations (specific nursing interventions to that disease). in some cases, they have broken the manifestations (signs and symptoms) of the pathophysiology down by body system which is really helpful--they do it in the section on renal failure. the book has charts, diagrams and two sections with color plates. i particularly like the step-by-step explanation that it gives for the progression of heart failure, something that is often a great mystery and difficult to understand. this book is part of a series; the other 3 are on assessment, pharmacology and signs & symptoms. i have the assessment and signs & symptoms books. they all kind of coordinate with each other--what i mean is that a lot of the same information is in them if it is appropriate to the subject of the book. the cost of these books is around $45. i am finding that i like the signs & symptoms book because it has some information on what to assess for, as well as treatment, which can be turned into nursing interventions, when confronted with a specific sign or symptom. very helpful with writing care plans on medical patients. it also gives you the specific medical diseases that a symptom is known to be a component of. sorry if i digressed a bit here.

Michelle123 · Jun 15, 2008

Thanks!

I'll look into the 2 in 1 series!

Michelle123 · Jun 15, 2008

I'm thinking, when I am on my final clinicals, that I will look at writing as many care plans as I can on as many of my pt's as possible.

We don't tend to do care plans on the wards here - we either have a single double sided sheet with boxes for each system and what needs to be done, such as how often vital signs, how often BSL's etc or we have this "clinical pathway" thing which is really helpful because it outlines what a person should be up to post surgical, I work on an ortho floor so they would indicate what a pt should be doing day one post op for a knee replacement so to speak. It allows for certain deviations etc as well. The only problem is, I actually asked the other staff where the clinical pathways were, and they don't keep them on the floor!

But I personally find things like clinical pathways and care plans really helpful for my learning. it reinforces which things to look out for, what to monitor and when to intervene, and what interventions to take. Although we don't use NANDA here.

Daytonite, BSN, RN · Jun 16, 2008

Sounds cool. I'd get my hands on as many clinical pathways as I could. A clinical pathway is just another style of a written care plan merged with nursing notes. One thing any care plan does do is memorialize in writing the critical thinking that goes into the problem solving of the nursing problems on that particular plan of care. There is no law or formal mandate by any accrediting organization that NANDA must be used as the way to identify nursing problems. The only requirement is that there is a care plan [Medicare Conditions of Participation 42CFR482.23(b)(4)] and that it be a part of the patient's medical record [JCAHO Comprehensive Accreditation Manual for Hospitals Standard IM 6.20, Elements of Performance 1]:

42CFR482.23(b)(4) - The hospital must ensure that the nursing staff develops, and keeps current, a nursing care plan for each patient.
JCAHO, Standard IM 6.20 - Records contain patient-specific information, as appropriate, to the care, treatment, and services provided. Elements of Performance 1. Each medical record contains, as applicable, the following clinical/case information: All reassessments and plan of care revisions, when indicated.

The choice to use nursing diagnoses, and specifically NANDA's nursing diagnosis taxonomy, is a decision made by each facility. Before NANDA we simply wrote out patient problems and they were often just symptoms. It took a group of smarty pants (sorry if I'm making it sound snotty) to say, "you know, I'm having to write the same interventions for this group of problems. Since they are all related, why don't we group them together and put one label on them and save ourselves a lot of repetitive writing." And, NANDA was born and changed our lives forever. The idea of NANDA was to standardize all this writing of problems on care plan forms. Why sit there and have to think about the way to word these things? That's what we had to do pre-NANDA. NANDA has pretty much done all the wording for you. But, if people weren't told that or never figured this out, they'll tell you how much they hate it. They should have been around back in 1970. NOC has given us outcomes and NIC the interventions that merge with the NANDA diagnoses. Added bonus is they can be programmed into a computer and you can just check the stuff off on a computer screen. We didn't have computers back in the 70's either and hand wrote all care plans.

The clinical pathways are no different, just a different format that sometimes incorporates NANDA diagnoses and sometimes doesn't. But it always reflects that the nursing process is being done and that a plan of care has been activated.

At the foundation of them all, however, is the nursing process which, as I constantly write, is nothing more than how we solve the problem using our tools of the nursing profession. Know the steps of the nursing process and what you have to do at each step and you can walk into any nursing facility and write a care plan using whatever crazy format they want you to use.

Assessment (collect data from medical record, do a physical assessment of the patient, assess ADL's, look up information about your patient's medical diseases/conditions to learn about the signs and symptoms and pathophysiology)
Determination of the patient's problem(s)/Nursing diagnosis (make a list of the abnormal assessment data, match your abnormal assessment data to likely nursing diagnoses, decide on the nursing diagnoses to use)
Planning (write measurable goals/outcomes and nursing interventions)
Implementation (initiate the care plan)
Evaluation (determine if goals/outcomes have been met)

Have fun working on your scenarios! There is a summary of threads with pathophysiology information collected together on it here: https://allnurses.com/forums/2634117-post49.html