My insulin Log

I.Patient’s Profile

General Data

NameF.B.
Age59 years old
SexMale
Civil StatusMarried
OccupationHousewife

History of Present Illness

The patient has a known case of Rheumatic Heart Disease (RHD). Patient underwent Mitral Valve Repair (MVR) in 1999 and has been on Coumadin therapy with no regular follow up of bleeding parameters.
Six days prior to admission, patient experienced headache and dizziness, but no consult was made. Instead, patient self-medicated with Bonamine which afforded relief.
Three days prior to admission, headache persisted with increased severity, which prompted patient to seek medical assistance at FEU Hospital. Mobic and Iterax were given.
Few hours prior to admission, patient was noted to have changes in sensorium and relatives decided to seek consult at Philippine Heart Center.
Upon admission, patient was noted to be unresponsive, stuporous, and speechless, with GCS of 7 (E2V1M4).

Past Medical History

The patient has denies any history of Diabetes Mellitus and Hypertension. As mentioned, she had a history of Rheumatic Heart Disease and had Mitral Valve Repair in 1999. She is a non-smoker and non alcoholic drinker.

Nursing Assessment (Problem-Based)

Neurologic:
LOC: drowsy to stuporous, 3-4 mm pupil size anisocoric, with brisk reaction to light; GCS – 9 (E4- Spontaneous eye opening V1- none/mechanical ventilation M4 – withdraws to pain) (+) doll’s eye reflex (+) babinski on right foot (-) corneal reflex, no visual threat

Respiratory
Patient is hooked to a mechanical ventilator through a tracheostomy. Ventilator set-up: 350/30/14/AC/5. (+) crackles on both lung fields. With equal breath sounds.

Cardiac
With atrial fibrillation; fine course, with occasional unifocal PVC’s. HR = 97 BP= 120’s-130’s/60’s-70’s.

Musculo-Skeletal
No contractures noted but there was stiffness noted at the right wrists and both ankle joints; with normal muscle tone and non-spontaneous movement; with severe weakness on both upper and lower extremities.

Hematologic
Latest PTPA: INR = 1.02 Act = 98%

II.Anatomy and Physiology of the Brain

Blood Supply of the Brain

The blood supply of the brain derives from the aortic arch via the right innominate, left common carotid and left subclavian arteries. It includes the conducting and penetrating vessels.
The venous system draining the brain is divided into vertebral veins that receive blood from the cerebellum. The cerebral veins have no valves. All the veins of the brain terminate into dural sinuses.

External Brain Structures

The brain is grossly divided into three main areas: the cerebrum, the brain stem and the cerebellum.
The largest portion of the brain is the cerebrum. It consists of two hemispheres that are connected together at the corpus callosum. The cerebrum is often divided into five lobes that are responsible for different brain functions. The cerebrum’s surface—the neocortex—is convoluted into hundreds of folds. The neocortex is where all the higher brain functions take place.

The cerebellum lies in the posterior fossa, separated from the cerebrum by tentorium cerebelli. It exerts ipsilateral control. It has three principal lobes. The Flocculonodular lobe is part of the vestibular system. It controls muscle tone, equilibrium and body position. The Anterior lobe receives most of the proprioreceptive and interoceptive input from head and body. It controls automatic movements and coordination. The posterior lobe coordinates voluntary movement.

The ventricles

The ventricles are a complex series of spaces and tunnels through the center of the brain. They secrete cerebrospinal fluid, which suspends the brain in the skull. They also provide a route for chemical messengers that are widely distributed through the central nervous system.

Cerebrospinal fluid

Cerebrospinal fluid (CSF) is a colorless liquid that bathes the brain and spine. It is formed within the ventricles of the brain, and it circulates throughout the central nervous system. It fills the ventricles and meninges, allowing the brain to “float” within the skull.

The Meninges

The meninges are layers of tissue that separate the skull and the brain.
The Dura mater is the tough and fibrous membrane. The Arachnoid membrane is the delicate membrane and contains subarachnoid fluid. Pia mater is the vascular membrane.
The subarachnoid space is fprmed by the arachnoid membrane and the pia mater.

Normal Flow of Cerebrospinal Fluid
Cerebrospinal fluid is produced in the Choroid plexuses of the ventricle. It flows from the lateral ventricles to the third ventricle passing through the interventricular foramen. Then it goes through the cerebral aqueduct to the fourth ventricle. From there fluid flows to the subarachnoid cisterns through the foramina of Magendie and Luschka to bathe the cerebral hemispheres. It exits through the saggital sinus to be absorbed by the arachnoid villi.

III.Pathophysiology of Subarachnoid Hemorrhage (SAH)

The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH comprises half of spontaneous atraumatic intracranial hemorrhages, the other half consist of bleeding that occurs within the brain parenchyma. Intracranial hemorrhage as a whole comprises 20% of all strokes.
Nontraumatic SAH usually is the result of a ruptured cerebral aneurysm or AVM. Blood extravasation into the subarachnoid space has a detrimental effect on both local and global brain function and leads to high morbidity and mortality rates.
The classic clinical picture of SAH is marked by the onset of very severe headache, tagged as the “worst in life”. Other associated signs and symptoms are loss of consciousness, seizures, diplopia and focal neurologic signs.
The early complications of SAH are rebleeding and hydrocephalus. Other complications include vasospasm, neurologic deficits, hypothalamic dysfunction and hyponatremia. Vasospasm from arterial smooth muscle contraction is symptomatic in 36% of patients. Neurologic deficits from cerebral ischemia peak at days 4-12. Hypothalamic dysfunction causes excessive sympathetic stimulation, which may lead to myocardial ischemia or labile detrimental BP. Hyponatremia may result from cerebral salt wasting (SIADH). Nosocomial pneumonia and other complications of critical care may occur.

Pathophysiology Diagram

Pathological Cycle Resulting from Increased Intracranial Pressure

Surgical Treatment

Ventriculo-peritoneal Shunting

The ventriculo-peritoneal shunt diverts CSF from a lateral ventricle or the spinal subarachnoid space to the peritoneal cavity. A tube is passed from the lateral ventricle through an occipital burr-hole subcutaneously through the posterior aspect of neck and paraspinal region to the peritoneal cavity through a small incision in the right lower quadrant.

IV.Nursing Diagnoses

1.Ineffective Breathing Pattern r/t neuromuscular impairment
2.Ineffective airway clearance related totracheobronchial secretions
3.Altered Level of Consciousness r/t decreased cerebral perfusion
4.Impaired Physical Mobility r/t neuromuscular impairment
5.Risk for Injury r/t possible shunt malfunction
6.Risk for Infection r/t post-surgical wound

V.Discharge Care Plan (METHODS)

MEDICATION
•Reinforce importance of medication compliance to patient and her relatives; its time, frequency, duration dosage and route.
•Advice to report unusual manifestations and side effects of drugs to physician.
•Monitor and evaluate effectiveness of medication regimen.

ENVIRONMENT/ EXERCISE
•Instruct patients watcher to provide calm and non stressful environment to prevent stimuli that could lead to seizures and an increase in Intracranial Pressure
•Advice to limit visitors
•Provide environment within normal room and body temperature.
•Maintain safe environment.
•Institute seizure precaution.
•Initiate positional precaution to prevent increase in intracranial pressure.
•Teach patient’s relative to perform passive range of motion exercises on patient’s extremities.

TREATMENT
•Teach patient’s relatives proper shunt care.
•Teach patient’s relatives how to suction properly.

HEALTH TEACHING ON DISEASE PROCESS
•Explain to patient’s relatives regarding patient’s neurological status and disease process, and its manifestations.
•Discuss possible complications of VP Shunt and its signs and symptoms

OUT PATIENT FOLLOW UP
•Inform relatives regarding importance of compliance on follow-up check up.
•In case of continued Coumadin therapy, stress the importance of regular PTPA monitoring.

Diet
•Refer to dietician for dietary instructions.

SPIRITUAL / SEXUAL
•Encourage patient’s relatives to seek spiritual support.
•Encourage patient’s husband on alternative ways on showing affections such as hugs and kisses.

XI.Bibliography

Nolte, J. The Human Brain: An Introduction to Its Functional Anatomy, Fifth Edition., Mosby, 2002. ISBN: 0-323-01320-1

Stoler, D. Coping with Mild Traumatic Brain Injury, Avery Penguin Putnam, 1998. ISBN: 0895297914

Human Anatomy and Physiology, Fifth Edition., 2000. ISBN: 0805349898.

Zuccarello, M. and McMahon, N. “Subarachnoid Hemorrhage”. www.mayfield.com, June 2004.

Rinkel GJ, Prins NE, Algra A. “Outcome Of Aneurysmal Subarachnoid Hemorrhage In Patients On Anticoagulant Treatment.” www.pubmed.gov, August 28, 2000.

Newton, Todd R., Subarachnoid Hemorrhage. Emedicine from WebMD. www.emedicine.com., December 19, 2005.