Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care

Book Description

Write individualized care plans with ease and confidence!
Product Description

Use this convenient resource to formulate nursing diagnoses and create individualized care plans! Updated with the most recent NANDA-I approved nursing diagnoses, Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care, 9th Edition shows you how to build customized care plans using a three-step process: assess, diagnose, and plan care. It includes suggested nursing diagnoses for over 1,300 client symptoms, medical and psychiatric diagnoses, diagnostik procedures, surgicalinterventions, and clinical states. Authors Elizabeth Ackley and Gail Ladwig use Nursing Outcomes Classification (NOC) and Nursing Interventions Classification (NIC) information to guide you in creating care plans that include desired outcomes, interventions, patient teaching, and evidence-based rationales.

Promotes evidence-based interventions and rationales by including recent or classic research that supports the use of each intervention.
Unique! Provides care plans for every NANDA-I approved nursing diagnosis.
Includes step-by-step instructions on how to use the Guide to Nursing Diagnoses and Guide to Planning Care sections to create a unique, individualized plan of care.
Includes pediatric, geriatric, multicultural, and home careinterventions as necessary for plans of care.
Includes examples of and suggested NIC interventions and NOC outcomes in each care plan.
Allows quick access to specific symptoms and nursing diagnoseswith alphabetical thumb tabs.
Unique! Includes a Care Plan Constructor on the companion Evolve website for hands-on practice in creating customized plans of care.

Includes the new 2009-2011 NANDA-I approved nursing diagnosesincluding 21 new and 8 revised diagnoses.
Illustrates the Problem-Etiology-Symptom format with an easy-to-follow, colored-coded box to help you in formulating diagnostic statements.
Explains the difference between the three types of nursing diagnoses.
Expands information explaining the difference between actual and potential problems in performing an assessment.
Adds detailed information on the multidisciplinary and collaborative aspect of nursing and how it affects care planning.
Shows how care planning is used in everyday nursing practice to provide effective nursing care.


Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care

Glasgow Coma Scale

Glasgow Coma Scale

The Glasgow Coma Scale provides a score in the range 3-15; patients with scores of 3-8 are usually said to be in a coma. The total score is the sum of the scores in three categories. For adults the scores are as follows:

Eye Opening Response	Spontaneous--open with blinking at baseline	4 points
	Opens to verbal command, speech, or shout	3 points
	Opens to pain, not applied to face	2 points
	None	1 point
Verbal Response	Oriented	5 points
	Confused conversation, but able to answer questions	4 points
	Inappropriate responses, words discernible	3 points
	Incomprehensible speech	2 points
	None	1 point
Motor Response	Obeys commands for movement	6 points
	Purposeful movement to painful stimulus	5 points
	Withdraws from pain	points
	Abnormal (spastic) flexion, decorticate posture	3 points
	Extensor (rigid) response, decerebrate posture	2 points
	None	1 point

Source : www.unc.edu

The 12 Cranial Nerves

There are 12 pairs of cranial nerves. These nerves arise from the brain and brain stem, carrying motor and or sensory information.

Cranial nerve I : Olfactory nerve

The olfactory nerve is composed of axons from the olfactory receptors in the nasal sensory epithelium. It carries olfactory information (sense of smell) to the olfactory bulb of the brain. This is a pure sensory nerve fiber.

Cranial nerve II: Optic nerve

The optic nerve is composed of axons of the ganglion cells in the eye. It carries visual information to the brain. This is a pure sensory nerve fiber. This nerve travels posteromedially from the eye, exiting the orbit at the optic canal in the lesser wing of the sphenoid bone. The optic nerves join each other in the middle cranial fossa to form the optic chiasm.

Cranial nerve III: Oculomotor nerve

The oculomotor nerve is composed of motor axons coming from the oculomotor nucleus and the edinger-westphal nucleus in the rostral midbrain located at the superior colliculus level. This is a pure motor nerve. It provides somatic motor innervation to four of the extrinsic eye muscles: the superior rectus, inferior rectus, medial rectus, and the inferior oblique muscles. It also innervates the muscles of the upper eyelid and the intrinsic eye muscles (the pupillary eye muscle.) Together, CN III, CN IV and CN VI control the six muscles of the eye.

Cranial nerve IV: Trochlear nerve

The trochlear nerve provides somatic motor innervation to the superior oblique eye muscle. This cranial nerve originates at the trochlear nucleus located in the tegmentum of the midbrain at the inferior colliculus level and exits the posterior side of the brainstem. It is also a pure motor nerve fiber.

Cranial nerve V: Trigeminal nerve

The trigeminal is the largest cranial nerve . It provides sensory information from the face, forehead, nasal cavity, tongue, gums and teeth (touch, and temperature) and provides somatic motor innervation to the muscles of mastication or “chewing”.

This cranial nerve has 3 branches: the ophthalmic, maxillary and mandibular branches.

It is composed of both sensory and motor axons. The sensory fibers are located in the trigeminal ganglion and the motor fibers project from nuclei in the pons.

Cranial nerve VI: Abducens nerve

The abducens nerve carries somatic motor innervation to one of the extrinsic eye muscles, the lateral rectus muscle. It is another pure motor nerve fiber and originates from the abducens nucleus located in the caudal pons at the facial colliculus level.

Cranial nerve VII: Facial nerve

The facial nerve carries somatic motor innervation to the many muscles for facial expression. It carries sensory information form the face (deep pressure sensation) and taste information from the anterior two thirds of the tongue. It arises at the pons in the brainstem and it emerges through openings in the temporal bone and stylomastoid foramen and has many branches. It is composed of both sensory and motor axons.

Cranial nerve VIII: Vestibulocochlear nerve

The vestibulocochlear nerve innervates the hair cell receptors of the inner ear. It carries vestibular information to the brain from the semicircular canals, utricle, and saccule providing the sense of balance. It also carries information from the cochlea providing the sense of hearing. This cranial nerve branches into the Vestibular branch (balance) and the cochlear branch (hearing). The cochlear fibers originate from the spiral ganglion. It is pure sensory nerve fiber.

Cranial nerve IX: Glossopharyngeal nerve

The glossopharyngeal nerve innervates the pharynx (upper part of the throat), the soft palate and the posterior one-third of the tongue. It carries sensory information (touch, temperature, and pressure) from the pharynx and soft palate. It carries taste sensation from the taste buds on the posterior one third of the tongue. It provides somatic motor innervation to the throat muscles involved in swallowing. It provides visceral motor innervation to the salivary glands. This cranial nerve also supplies the carotid sinus and reflex control to the heart . It is composed of both sensory and motor axons and originates from the nucleus ambiguous in the reticular formation of the medulla.

Cranial nerve X: Vagus nerve

The vagus nerve consists of many rootlets that come off of the brainstem just behind the glossopharyngeal nerve. The branchial motor component originates from the nucleus ambiguous in the reticular formation of the medulla. The visceral component originates from the dorsal motor nucleus of the vagus located in the floor of the fourth ventricle in the rostral medulla and in the central grey matt er of the caudal medulla. It is the longest cranial nerve

innervating many structures in the throat, including the muscles of the vocal cords, thorax and abdominal cavity. It provides sensory information (touch, temperature and pressure) from the external auditory meatus (ear canal) and a portion of the external ear. It carries taste sensation from taste buds in the pharynx. It also provides sensory information from the esophagus, respiratory tract, and abdominal viscera (stomach, intestines, liver, etc.). It provides visceral motor innervation to the heart, stomach, intestines, and gallbladder. It is part of the ANS, the parasympathetic branch. It is composed of both sensory and motor axons. Other parasympathetic ganglia include CN III , CN VII and CN IX .

Cranial nerve XI: Spinal Accessory nerve

The spinal accessory nerve has two branches. The cranial branch provides somatic motor innervation to some of the muscles in the throat involved in swallowing. This cranial branch is accessory to CN X, originating in the caudal nucleus ambiguous, with the fibers of the cranial root traveling the same extracranial path as the branchial motor component of the vagus nerve. The spinal branch provides somatic motor innervation to the trapezius muscles, providing muscle movement for the upper shoulders head and neck. It is pure motor nerve fiber.

Cranial nerve XII: Hypoglossal nerve

The hypoglossal nerve provides somatic motor innervation to the muscles of the tongue. This pure motor nerve originates from the hypoglossal nucleus located in the tegmentum of the medulla.

Source : www.pitt.edu

Level of Consciousness

The normal state of consciousness comprises either the state of wakefulness, awareness, or alertness in which most human beings function while not asleep or one of the recognized stages of normal sleep from which the person can be readily awakened.

The abnormal state of consciousness is more difficult to define and characterize, as evidenced by the many terms applied to altered states of consciousness by various observers. Among such terms are: clouding of consciousness, confusional state, delirium, lethargy, obtundation, stupor, dementia, hypersomnia, vegetative state, akinetic mutism, locked-in syndrome, coma, and brain death. Many of these terms mean different things to different people, and may prove inaccurate when transmitting and recording information regarding the state of consciousness of a patient. Nevertheless, it is appropriate to define several of the terms as closely as possible.

Clouding of consciousness is a very mild form of altered mental status in which the patient has inattention and reduced wakefulness.

Confusional state is a more profound deficit that includes disorientation, bewilderment, and difficulty following commands.

Lethargy consists of severe drowsiness in which the patient can be aroused by moderate stimuli and then drift back to sleep.

Obtundation is a state similar to lethargy in which the patient has a lessened interest in the environment, slowed responses to stimulation, and tends to sleep more than normal with drowsiness in between sleep states.

Stupor means that only vigorous and repeated stimuli will arouse the individual, and when left undisturbed, the patient will immediately lapse back to the unresponsive state.

Coma is a state of unarousable unresponsiveness.

It is helpful to have a standard scale by which one can measure levels of consciousness. This proves advantageous for several reasons: Communication among health care personnel about the neurologic condition of a patient is improved; guidelines for diagnostic and therapeutic intervention in certain situations can be linked to the level of consciousness; and in some situations a rough estimate of prognosis can be made based partly on the scale score. In order for such a scale to be useful it must be simple to learn, understand, and implement. Scoring must be reproducible among observers. The Grady Coma Scale has proved functional in this regard. It has been used for more than 10 years at Grady Memorial Hospital in Atlanta, Georgia, to gauge the level of consciousness of patients in the neurosurgical intensive care unit and elsewhere. The grade I patient is only slightly confused. The grade II patient requires a light pain stimulus (such as a sharp pin tapped lightly over the chest wall) for appropriate arousal, or may be combative or belligerent. The grade III patient is comatose but will ward off deeply painful stimuli such as sternal pressure or nipple twist with an appropriate response. The grade IV patient reacts inappropriately with either decorticate or decerebrate posturing to such deeply painful stimuli, and the grade V patient remains flaccid when similarly stimulated.

Pathophysiology of Congestive Heart Failure (CHF)

Congestive Heart Failure (CHF)


Congestive heart failure, or heart failure, is a condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from "backing up" into the lungs.


In most cases, heart failure is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ. Heart failure is characterized by shortness of breath (dyspnea) and abnormal fluid retention, which usually results in swelling (edema) in the feet and legs.


Pathophysiology of Congestive Heart Failure (CHF)


Heart failure occurs, the body undergoes some adaptation, both in heart and systemically. If the stroke volume of both ventricles is reduced, because of pressure contractility, or afterload are greatly increased, the volume and pressure at the end of diastolic heart in two space will increase. This will increase the end diastolic myocardial fiber length, causing systolic time becomes shorter. If this condition lasts long, there was dilatation of the ventricles. Cardiac output at rest can still be good, but the increase in diastolic pressure that persists / chronicle will spread to both the atrium and the pulmonary circulation and systemic circulation.


Finally, capillary pressure will increase which will cause fluid transudation and pulmonary edema or systemic edema. Decrease in cardiac output, especially if associated with a decrease in arterial pressure or decreased renal perfusion, will activate several neural and humoral systems. Increased activity of the sympathetic nervous system will stimulate myocardial contraction, heart rate and venous; changes that last time, will increase central blood volume which in turn increases the preload.


Although the adaptation was designed to increase cardiac output, the adaptation itself can interfere with the body. Therefore, tachycardia and increased myocardial contractility stimulated the occurrence of ischemia in patients with previous coronary artery disease and increased preload may worsen pulmonary congestion.


Activation of the sympathetic nervous system will also increase peripheral resistance, this adaptation designed to maintain perfusion to vital organs, but if the activation is greatly increased, will decrease the flow to the kidneys and tissues. Peripheral vascular resistance may also be the main determinant of ventricular afterload, so that excessive sympathetic activity can improve heart function. One important effect is the decrease in cardiac output decreased renal blood flow and decrease in filtration velocity glomerolus, which will cause sodium and fluid retention.


System renin - angiotensin - aldosterone also be activated, causing further increase in peripheral vascular resistance and increased left ventricular afterload as sodium and fluid retention. Heart failure is associated with increased levels of arginine vasopressin in the circulation increases, which also is vasokontriktor and inhibiting the excretion of fluids. In heart failure atrial natriuretic peptide increased due to increased atrial pressure, which indicates that there is resistance to the effects of natriuretic and vasodilator.

Pathophysiology of Dengue Hemorrhagic Fever

Pathophysiology of Dengue Hemorrhagic Fever

Dengue hemorrhagic fever

Dengue hemorrhagic fever is a severe, potentially deadly infection spread by certain species of mosquitoes (Aedes aegypti).

Pathophysiology of Dengue Hemorrhagic Fever

Dengue viruses enter the body through the bite of aedes aegypti mosquito and then react with the antibody and virus-antibody complexes formed, the circulation will activate the complement system.

Dengue viruses enter the body through mosquito bites and infection first causes dengue fever. Body reaction is a reaction commonly seen in infection by the virus. A very different reaction would appear, if someone gets recurrent infections with different dengue virus type. And Dengue hemorrhagic fever can occur when a person after infection the first time, get recurrent infections other dengue virus. Re-infection will cause an anamnestic antibody response, causing the concentration of antigen-antibody complex is high.

Pathophysiology of Diabetes MellitusType 1

Pathophysiology of Diabetes MellitusType 1

Insulin is essential to process carbohydrates, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen (glycogenesis) as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. It also stimulates fat storage. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in both liver and kidneys.

Hyperglycemia (ie, random blood glucose concentration more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to diabetic ketoacidosis (DKA).

The effects of insulin deficiency are shown in the image below.


An excess of insulin prevents the release of glucose into the circulation and results in hypoglycemia (blood glucose concentrations of < 60 mg/dL or 3.5 mmol/L). Glucose is the sole energy source for erythrocytes, kidney medulla, and the brain. Source :emedicine.medscape.com

Pathophysiology of Coronary artery disease

Coronary artery disease (CAD) also known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease, or ischemic heart disease (IHD), is the most common type of heart disease and cause of heart attacks. The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the arteries and reduces blood flow to the heart.

Angina (chest pain) that occurs regularly with activity, after heavy meals, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with betablocker therapy such as metoprolol or atenolol. Nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms are also effective in relieving symptoms but are not known to reduce the chances of future heart attacks. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction. About 80% of chest pains have nothing to do with the heart.

This condition is chronic and begins when a person is an adolescent and then it slowly progresses throughout their life. Coronary artery disease pathophysiology revolves around a few theories. One widely accepted theory is that this condition occurs when the body is trying to heal itself as a result of endothelial injury. Inflammation is also beginning to be accepted as a critical component of potential plaque instability and atherosclerosis activity. Patients who have been diagnosed with established coronary artery disease and have several of the causes and/or risk factors as well are at a much higher risk of experiencing a cerebrovascular accident, myocardial infarction, and other vascular events in the future.

Elevated C-reactive protein levels, and other elevated biochemical markers, indicate a higher risk of experiencing a vascular event in the future and it indicates an increased likelihood of vascular inflammation. This marker may also indicate the need for aggressive preventative measures due to the patient having a quickly advancing coronary artery disease.

How to Prevent Your Baby from Developing Plagiocephaly

Plagiocephaly or flat head syndrome in babies is a growing concern today. Many babies tend to develop flat heads during their initial months of birth. This article tells you about plagiocephaly and methods to prevent it.



A new born baby has a soft and delicate head due to which it tends to develop a deformity because of continuous pressure. The deformity usually occurs as a flat spot on the baby's head. Development of such a deformity in new born babies is known as plagiocephaly or flat head syndrome. This syndrome is usually seen when babies spend more time lying down in one position for a long time which results in continuous exertion of pressure on that particular area, ultimately resulting in a flat spot. A flat head can also be a result of pressure exerted on the baby's head during its passage from the birth canal during vaginal delivery. Such deformities tend to rectify within six weeks after birth.


Increased incidence of Sudden Infant Death Syndrome (SIDS) lead to "Back to Sleep" campaign under which parents were instructed to make their babies sleep on their back. Practicing this approach definitely reduced the occurrence of SIDS however, it lead to increased incidence of flat heads among babies. Even though this deformity does not cause brain damage, it is a cause of concern.


Prevention of Plagiocephaly

The most common form of plagiocephaly is positional plagiocephaly. When a baby is placed on the mattress with its face up for a long time, it develops positional plagiocephaly due to continuous pressure on a particular area of the head. As babies are incapable of moving their heads in different directions, pressure on a single area leads to the development of a flat spot. Now the question is - How to prevent plagiocephaly in babies? Here is the answer.

Include a fair amount of "tummy time" when your baby is awake. Mothers should make their babies practice to be on their tummy because many babies do not like it. Starting their tummy time right away will help them develop a habit of spending time on their tummy.
Make your baby spend time in other positions like being upright or lying on its side. This will let your baby experience other positions and help discovering the world around it in a different way.
Changing your baby's position throughout the day will also help in preventing plagiocephaly.
Do not place your baby on a car seat or baby swing for long, as this adds to the time of pressure exerted on the baby's head.
You can spend more time carrying your baby on a sling throughout the day. Babywearing is a nice way of reducing the amount of time the baby spends on its back. This not only increases the total time you spend with your baby, it will also be a treat for your little one to enjoy your company!
Keep changing the direction of your baby's head while sleeping. This will prevent the baby from keeping its head tilted in one direction for long.
Place a baby pillow underneath you baby's head during sleeping. Such pillows distribute the pressure evenly and prevent babies from developing flat heads.
Feed your baby by placing it on both the sides alternatively. This will decrease the time spent in one position and reduce the chances a flat head.

Another form of plagiocephaly is craniosynostosis in which, the joints of the skull close early resulting in improper growth of brain. Surgical treatment is required to treat this birth defect. A baby with a flat spot on the head needs medical attention. Parents must immediately contact a pediatrician if they observe a flat spot developing on their baby's head. Depending on severity of the condition, doctor will advise a treatment. Severe cases call for cranial orthotic therapy in which the baby is made to wear aplagiocephaly helmet for 23 hours a day for a period of 2-6 months to correct the shape of baby's head. It is advisable, that parents start practicing the preventive measures for plagiocephaly so that the need for treatment does not arise at all.

By Priyanka Sonkushre

Normal Weight in Pounds for Pediatric

Weight in pounds: Weight is another important factor where the health of children is concerned. Weight in pediatrics, especially of the newborns is recorded in pounds. So what is the normal range of weight for children? Here is an overview of the normal weight of an individual at each stage from birth to adulthood.

Newborn: The normal weight of a new born is between 4.5 to 7 pounds. If its premature, then the weight can be lesser.
Infant: An infant normally weighs between 9 and 22 pounds.
Toddler: At this age usually children grow very rapidly. So the normal weight for a toddler is between 22 and 31 pounds.
Pre-school children: Pre school children again, are at a stage where they grow very fast. So the normal weight for them could fluctuate anywhere around 14 and 18 pounds.
School going children: School children are in a stage of flux. They are running around, doing a lot of physical activities and create trouble for their mothers! But on a serious note, school going children weigh some where around 40 and 90 pounds.
From 12 years to adulthood: The stage of transformation of children to adults is a very complex one. There are a lot of bodily changes during this stage and the normal weight for this age group is anywhere around the same as school going children, although slightly more. It hovers between 90 and 100 pounds.

Normal Weight in Pounds for Pediatric

Normal Heart Rate for Pediatric

Heart Rate: Heart rate is always recorded in heart beats per minute. Too high or too low number of heartbeats per minute can be problematic. Check out what are the normal ranges of this vital signs on children and infants.

• Newborn: For a newborn, the heart rate is between 80 and 180. The average or the mean is 140.
• Infant: As the baby grow, the heart rate decreases. An infant has a heart rate of 70-170 heartbeats per minute and the mean is around 135.
• Toddler: Normal heart rate for a toddler is 90-150. There could be a slight variation, according to the constitution, which could mean that the mean heart rate for a toddler is 120.
• Pre-school children: In pre-school children, the heart beats per minute vary between 65 and 135. The mean heart rate for pre-school children is 110.
• School Children: Normal heart rate is for school going children is between 60 and 120. The mean fluctuates between 85 to 100 for pre-school children.
• From 12 years to adulthood: The individuals who are 12 years and above, and even adults have a heart rate between 60 and 100. In the adults the mean of this rate is between 80 and 85.

Normal Heart Rate for Pediatric

Normal Respiratory Rate for Pediatric

Respiratory Rate: Respiratory rate is a one of the very important pediatric vital signs. It checks the breaths of an individual per minute.

• Newborn: Ideally a new born should not be recording more than 30 to 60 breaths per minute. In case it is not, well, then, there could be a problem.
• Infant: An infant can be supposed to be normal if it is between 30 to 50 breaths per minute.
• Toddler: A toddler has a respiratory rate of 24 to 40 breaths per minute.
• Pre-school children: Pre school children have an even lower respiratory rate. The maximum breaths per minute school children have is around 35 and the least is 22 breaths per minute.
• School Children: A normal respiratory rate for the school children is even lesser. It is between 16 to 30 breaths per minute.
• From 12 years to adulthood: From 12 years and above, Adults have a respiratory rate of between 12 and 20 breaths per minute.

Normal Respiratory Rate for Pediatric

Normal Systolic Blood Pressure for Pediatric

Normal Systolic Blood Pressure for Pediatric

This, in a layman's term is the lower limit of blood pressure. It is the blood pressure on the walls of the blood vessels when the heart chambers contract while driving the blood out of the heart. So lets check out age wise what should be the normal range of systolic blood pressure.

• Newborn: For a new born baby to be diagnosed as normal, the systolic blood pressure should be between 50 and 70 mm Hg. If its not, then, an alarm could probably ring in the doctor's mind.
• Infant: If an infant is the subject of a check up for systolic blood pressure, then, the normal range of blood pressure should be between 70 mm Hg.
• Toddler (1-3years): A perfectly normal systolic blood pressure for a toddler would be again in the same range as the infant, but a bit higher. Ideally it should be around 70-76mm Hg.
• Pre-school age: A child of a preschool age, that is between 3 to 5 years, is around 80 mm Hg.
• School Children: Children who are in the age group between 5 and 12, have systolic blood pressure in the range of 80 and 90 mm Hg.
• From 12 years to adulthood: By this time the individual acquires the full range of the systolic blood pressure, which varies from 100 and 120.

In most of the cases, the blood pressure cannot be checked as the arms of the babies and infants and even pre school children are too small to be fitted into the blood pressure apparatus. So many a times, blood pressure can be measured properly once the kid is around 10 years old.