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Eating Disorders in Children and Adolescents

EATING DISORDERS

Eating disorders are conditions characterized by an extreme disturbance in eating related behaviour.

Eating disorders are moderate to severe illnesses that are characterized by disturbances in thinking and behaviour around food, eating and body weight or shape.

The DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Association,
2013) outlines six types of disordered eating patterns but four types are commonly diagnosed:

Anorexia Nervosa (AN)
Bulimia Nervosa (BN)
Binge Eating Disorder (BED)
Avoidant Restrictive Food Intake Disorder (ARFID)

The rest of the two types are;

5. Other Specified Feeding or Eating Disorders (OSFED)
OSFED is also a moderate to severe illness and may include eating disorders of clinical significance that do not meet the criteria for AN or BN. OSFED and USFED may be as severe as AN or BN.
6. Unspecified Feeding or Eating Disorders (USFED)
USFED applies to where behaviours cause significant distress or impairment of functioning, but do
not meet the full criteria of any of the other feeding or eating disorder criteria.

ANOREXIA NERVOSA

Anorexia nervosa (AN) is a severe eating disorder characterized by a distorted body image that leads to restricted eating, over exercise and other behaviors that prevents a person from gaining weight or
maintaining a healthy weight.

Anorexia Nervosa is defined as self-induced starvation resulting from fear of gaining weight rather than from true loss of appetite.

Person with anorexia nervosa continues to feel hunger but persists in denying himself or her self food.

Children and teens with anorexia have a distorted body image. People with anorexia view themselves as heavy, even when they are dangerously skinny. They are obsessed with being thin and refuse to maintain even a minimally normal weight.

Signs and Symptoms of Anorexia Nervosa

Refusal to maintain a minimum normal body weight.
Is intensely afraid of gaining weight.
Significant disturbance in the perception of the shape or size of his or her body.(distorted image)
Dieting even when one is thin or emaciated
The individual maintains a body weight that is below a minimally normal level for age and weight.
They exclude from their diet what they perceive to be highly caloric foods. ie they restrict diet.
Purging i.e. self-induced vomiting or misuse of laxatives, diuretics.
There is excessive exercise to reduce weight.
Reduced total food intake
Intense fear of becoming fat or obese.
Strange eating habits, very picky.
Infrequent menstruation or Amenorrhea due to reduced estrogen and loss of weight
Oligomenorrhoea or failure to reach menarche.
Loss of sexual interest
Anxiety, depression, perfectionism(hold themselves to impossibly high standards)

Possible complications of Anorexia Nervosa

Anorexia nervosa is fatal in about 10% of cases. Most common death from anorexia nervosa is due to, cardiac arrest, electrolyte imbalance and suicide.

Heart muscle damage that can occur as a result of malnutrition or repeated vomiting may be life threatening.
Arrhythmias (a fast, slow, or irregular heartbeat)
Hypotension (low blood pressure)
Electrolyte imbalance.
Anaemia (low RBC’s) and Leukopenia(low WBC’s)
GIT disturbances.
Dehydration
Refeeding Syndrome,
Refeeding Syndrome “is potentially a fatal condition defined by severe electrolyte and fluid shifts as a result of a rapid reintroduction of nutrition after a period of inadequate nutritional intake

Management or Treating Anorexia Nervosa

Refer to General Management,

The major aim of treatment is to bring the young person back to normal weight and eating habits.
Hospitalization, sometimes for weeks, may be necessary. In cases of extreme or life-threatening malnutrition, tube or intravenous feeding may be required.

Nursing care

Short term management is focused on ensuring weight gain and correcting nutritional deficiencies. maintaining normal weight and preventing relapses
provide a balanced diet of at least 3000 calories in 24 hours
a nurse should always supervise the patient during meals
patient should be under complete bed rest initially under nurses observation so as to achieve a weight gain goal of 0.5 to 1kg per week
control vomiting by making the bathroom inaccessible 2 hours after food
in extreme cases when the patient refuses to comply with treatment and eating, gavage feeding may need to be instituted
weight should be checked regularly and plotted on a weight chart
maintain a strict intake and output chart
monitor skin status and oral mucous membrane for signs of dehydration
encourage patient to verbalise feelings of fear and anxiety related to the achievement
encourage family to participate in education regarding patients disorder
avoid discussions that focus on food and weight

Long-term treatment addressing psychological issues include:

antidepressant medication
Neuroleptics
appetite stimulants
behavioral therapy
individual therapy
cognitive behavioural therapy
family therapy
psychotherapy
support groups

BULIMIA NERVOSA

Bulimia nervosa, or bulimia, is a type of eating disorder in which a person engages in episodes of bingeing—during which he or she eats a large amount of food—and then purges, or tries to get rid of the extra calories.

Bulimia nervosa is a syndrome of episodes of binge eating followed by self-induced vomiting or purge behaviour accompanied by an excessive pre occupation with weight and body shape.

Young people with bulimia try to prevent weight gain by inducing vomiting or using laxatives, diet pills, diuretics, or enemas. After purging the food, they feel relieved. Binge eating is often done in private. Because most people with bulimia are of average weight or even slightly overweight, it may not be readily apparent to others that something is wrong.

The condition often begins in the late teens or early adulthood and is diagnosed mostly in women. People with bulimia may have other mental health issues, including depression, anxiety, drug or alcohol abuse, and self-injurious behaviors.

Doctors make a diagnosis of bulimia after a person has two or more episodes per week for at least three months. People with bulimia usually fluctuate within a normal weight range, although they may be overweight, too. As many as one out of every 25 females will have bulimia in their lifetime.

Binge is eating in a discrete period of time an amount of food that is definitely larger than most individuals would eat under similar circumstances.

Signs and Symptoms of Bulimia Nervosa

The individual is typically ashamed of his or her eating problem.
Persistent heart burn and sore throat.
Abdominal and epigastric pain.
They tend to conceal their symptoms, It occurs in secrecy
Food is consumed rapidly
Binge eating continues until the individual is uncomfortable or even painfully full.
The binge eating is usually triggered by low mood, interpersonal stressors, intense hunger
following dietary restraint.
Loss of self control, Difficult in resisting binge eating or difficult in stopping it.
Employs compensatory technique for example induce vomiting after binge eating.
They place emphasis on body shape and weight in their self evaluation.
Have fear in losing weight.
May be overweight or underweight
Low self esteem
Increased frequency of anxiety for example fear of social situation
Fluid and electrolyte imbalance due to purging
Menstrual irregularity or amenorrhea may occur
Rectal prolapse
Increased dental caries
Scarring of knuckles from using fingers to induce vomiting.

Management or Treating Bulimia Nervosa

Refer to General Management,

Treatment aims to break the binge-and-purge cycle. Treatments may include the following:

Nursing care

engage patient in therapeutic alliance to obtain commitment to treatment
establish contract with the patient that specifies amount and type of food she must eat at each meal
set a time limit for each meal
identify patients elimination patterns
encourage the patient to recognize and verbalize her feelings about her eating behavior
explain the risks of laxative, emetic and diuretic abuse
assess and monitor patients suicide potential

Other treatment modalities

antidepressants medication
behavior modification
individual, family, or group therapy
nutritional counseling
self help groups

Complications of Bulimia Nervosa

Stomach acids from chronic vomiting can cause,
damage to tooth enamel,
inflammation of the esophagus,
swelling of the salivary glands in the cheeks,
low potassium which can lead to abnormal heart rhythms.

BINGE EATING DISORDER

Binge eating is similar to bulimia.

Binge eating refers to chronic, out-of-control eating of large amounts of food in a short time, even to the point of discomfort without purging the food through vomiting or other means.

People with binge eating disorder eat unusually large amounts of food often and in secret but do not attempt to get rid of calories once the food is consumed. People with the condition may be embarrassed or feel guilty about binge eating, but they feel such a compulsion that they cannot stop.

These people can be of average weight, overweight, or obese. They may also have other mental health disorders, such as depression. Many binge eaters have trouble coping with anger, sadness, boredom, worry, and stress.

Binge eating disorder often has no physical symptoms, but it has psychological symptoms that may or may not be apparent to others, such as depression, anxiety, or shame or guilt over the amount of food eaten. Frequent dieting without weight loss is another symptom.

The excess weight caused by binge eating puts the child at risk of these health problems:

heart disease
high blood pressure
high cholesterol
type 2 diabetes

Treatments include the following: Refer to General Management,

behavioral therapy
medications, including antidepressants
psychotherapy

AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER

Avoidant/restrictive food intake disorder, is an eating disorder where a person is unable to or refuses to eat certain foods based on texture, color, taste, temperature, or aroma.

The condition can lead to weight loss, inadequate growth, nutritional deficiencies, and impaired psychosocial functioning, such as an inability to eat with others. Unlike anorexia nervosa, there are not weight or shape concerns or intentional efforts to lose weight.

For instance, a child may consume only a very narrow range of foods and refuse even those foods if they appear new or different. This type of eating disorder commonly develops in childhood and can affect adults as well.

Assessment/Screening for an Eating Disorder

The SCOFF Test:

Early detection in patients with unexplained weight loss improves prognosis and may be aided by use of the SCOFF questionnaire, developed by John Morgan at Leeds Partnerships NHS Foundation
Trust.

This questionnaire uses five simple screening questions and has been validated in specialist and primary care settings. It has a sensitivity of 100% and specificity of 90% for anorexia nervosa. A score of 2 or more positive answers should raise your index of suspicion of a case, highlighting the need for a comprehensive assessment for an eating disorder and
consultation with an eating disorder expert or mental health clinician.

2. SUSS (Sit up – Squat – Stand Test) for muscle strength

1. Sit-up: patient lies down flat on the floor and sits up without, if possible, using their hands

2. Squat–Stand: patient squats down and rises without, if possible, using their hands.

Scoring (for Sit-up and Squat-Stand tests separately)

Parameter	Score
Unable	0
Able only when using hands to help	1
Able with noticeable difficulty	2
Able with no difficulty	3

A Sit up – Squat – Stand(SUSS) score ≤ 2 indicates a RED FLAG.

Anorexia Nervosa (AN) has the HIGHEST MORTALITY rate of ALL mental health illnesses
Patients with AN are at risk of sudden death if the have the RED FLAGS below.

RED FLAGS

SUSS score less or equal to 2
Postural drop
Bradycardia
Hypothermia
Electrolyte abnormalities

Nurses Role during assessment

Nurses in the hospital or primary care setting are in a crucial position to screen for and detect eating disorders, hence the importance for nurses to have an awareness of the indicators for eating disorder assessment.
supporting psychological based therapies, psycho-education regarding
effects of the eating disorder,
assessment of risk,
promoting recovery and hope,
involving famil and caretakers,
observing for co-morbidities.

GENERAL MANAGEMENT OF EATING DISORDERS

Aims

To restore the patient’s nutritional status.
To prevent complications.

General management

Develop a trusting relationship with the patient.
Convey positive regard to the patient
Stay with the patient especially at the time of meals and 1 hour after meals.
Avoid arguing or bargaining with the patient who is resistant to treatment.
State matters of facts which behaviours are unacceptable.
Encourage the patient to verbalize feelings regarding role within the family and issues related to dependence.
Help the patient to recognize ways to gain control over these problems in life.
Help the patient to develop a realistic perception of body image and relationship with food.
Promote feelings of control within the environment through participation and dependent
decision making.
Weigh patient daily. Always use the same weighing scale to avoid errors.
Keep strict record of observations especially fluid input and output.
Assess skin; motility and tugor regularly.
Assess moistness and color of the skin and oral mucus membranes.

Behaviour modification

Develop care plan together with the client
Encourage the client to sign a contract is necessary
Staff and client can agree on a system of reward.
Individual therapy such as psychotherapy may be important. This is particularly helpful when there is underlying psychological problems contributing to the maladaptive behaviour.
Family therapy:
> Counsel the family members. This includes educating the family about the disorder, assessing the family perception or attitudes.
> Support given to the family
Refer if necessary
Chemotherapy: there are no specific drugs indicated for the treatment of the condition. Drugs
such as flouxetine, chlorpromazine, and lithium carbonate have been used.

Nursing Diagnoses

Imbalanced nutrition less than body requirement related to refusal to eat or self induced vomiting as evidenced by loss of weight.
Ineffective denial related to fear of losing or retarded ego development as evidenced by inability to admit the impact of maladaptive eating behaviours on life pattern.
Disturbed body image related to false perception of increased body weight evidenced by patient’s verbalization of that she has global over weight.

Eating Disorders in Children and Adolescents Read More »

Disaster Preparedness and Management

DISASTER

Disaster is an occurrence disrupting the normal conditions of existence and causing a level of suffering that exceeds the capacity of adjustment of the affected community, WHO

Disaster is also defined as a sudden/unexpected catastrophic event causing serious disruption of the functioning of a community or society that exceed the ability of the affected community or society to cope using its own resources.

Key words used in Disaster

Vulnerability: Is lack of capacity to deal with potential threat. Lack of information, resources and technology. There are many
aspects of vulnerability, arising from various physical, social, economic, and environmental factors. Examples may include: poor design and construction of buildings, inadequate protection of assets, lack of public information and awareness, limited official
recognition of risks and preparedness measures, and disregard for wise environmental management
There are four (4) main types of vulnerability:
(a). Physical Vulnerability may be determined by aspects such as population density levels, remoteness of a settlement, the site, design and materials used for critical infrastructure and for housing. Example: Wooden homes are less likely to collapse in an earthquake, but are more vulnerable to fire.
(b). Social Vulnerability refers to the inability of people, organizations and societies to withstand adverse impacts to hazards due to characteristics inherent in social
interactions, institutions and systems of cultural values. It includes aspects related to levels of literacy and education, the existence of peace and security, access to basic human rights, systems of good governance, social equity, positive traditional values, customs and ideological beliefs and overall collective organizational systems Example: When flooding occurs some citizens, such as children, elderly and differently-able, may be unable to protect themselves or evacuate if necessary.
(c). Economic Vulnerability. The level of vulnerability is highly dependent upon the economic status of individuals, communities and nations i.e. the poor are usually more vulnerable to disasters because they lack the resources to build sturdy structures and put other engineering measures in place to protect themselves
from being negatively impacted by disasters. Example: Poorer families may live in squatter settlements because they cannot afford to live in safer (more expensive) areas.
(d). Environmental Vulnerability. Natural resource depletion and resource degradation are key aspects of environmental vulnerability. Example: Wetlands, such as the Caroni Swamp, are sensitive to increasing salinity from sea water, and pollution from storm water runoff containing agricultural chemicals, eroded soils, etc.
Disaster risk: Is the likelihood of specific hazard occupancy and its probable consequence for people, property and environment.
(a). Acceptable risk: The extent to which a disaster risk is deemed acceptable or tolerable depends on existing social, economic, political, cultural, technical and environmental conditions.
(b). Residual risk: is the disaster risk that remains even when effective disaster risk
reduction measures are in place, and for which emergency response and recovery
capacities must be maintained. T
Intensity: Refers to a disaster agent’s ability to inflict damage and injury.
Scope: Refers to the geographic area and social space dimension impacted by the disaster agent.
Frequency: Refers to the number of times certain disasters occur in certain geographical locations that may give time to the community to take measures in preparation.
Controllability: Refers to some control measures that can reduce the impact of the disaster. It helps the emergency planners.
Triage: Refers to sorting out victims according to the extent of severity.
Time: Refers to the period when certain disasters can last that can allow the affected people to vacate when there is a period of warning the community to vacate for protection.
Capacity: The ability of a community to use all the available resources that can reduce risk level and disaster effects.
Capacity building: It is the efforts to develop human skills within a community to reduce
risk levels.
Emergency: a state in which normal procedures are suspended and extra-ordinary measures are taken in order to avert a disaster, WHO.
Catastrophe: It is a large scope of impact event that affects multiple communities, produces very high levels of damage and social disruption, and sharply and concurrently interrupts community and lifeline services. A broad scope of impact impairs each community’s emergency response system and greatly limits extra community support.”
Hazard: A natural or human-made event that threatens to adversely affects human life, property or activity to the extent of causing a disaster.

Epidemiology of a disaster

Epidemiology is the study of patterns of a disease occurrence in human population and the factors that influence these patterns.

Epidemiology is divided into 3 parts namely i.e. Agent, host
and environment

DISASTER AGENT: The agent is the physical agent that actually causes the injury or destruction.
(a). Primary agents include; falling, building, heat, winds or using water.
(b). Secondary agents include; bacteria and viruses that produce contamination or infection after primary agents.
HOST: These are the characteristics of humans that influence several of the disaster effects e.g. ages, immune status, pre-existing health status, degree of morbidity and emotional stability. The individuals who are mostly affected are the pregnant mothers, the elderly and the children because they are vulnerable.
ENVIRONMENT: Environmental factors that affect outcome of disaster include; physical, chemical, biological and social factors.
(a). Physical factors include; the time when disaster occurs, weather conditions, availability of good water supply and functionality facilities and others for example communication system.
(b). Chemical factors. Influencing disasters include leakage of stored ground water or food supply that may directly affect human life when consumed.
(c). Biological factors are those that occur as a result of contaminated water, waste disposal, and improper food storage.
(d). Social factors are those factors that contribute to the individuals’ social support systems, loss of family members and changes in responsible roles.

Causes of Disasters

1. Geological and Climatic Changes: This causes disasters if they become extreme e.g. lack or insufficiency of rain for an extended period that severely disturbs the hydrologic cycle in an area.
2. Poverty: It generally makes people vulnerable to the impact of hazards because they settle on hills that are prone to landslide, along the riverside invaluably flood their banks
3. Population Growth: More people will be forced to live and work in unsafe areas which cause increasing numbers of people will be competing for limited amount of resources such as employment opportunities, and land which can lead to conflict; this conflict may result in crisis—induced migration thereby resulting in disasters.
4. Rapid Urbanization: It is characterized by rural poor moving to metropolitan areas in search of economic opportunities and security which may cause them not find safe and desirable places to build their houses that can lead to human-made disasters.
5. Transitions in Cultural Practices: This involves cultural Introduction of new construction material to build houses or materials used incorrectly may lead to house that cannot withstand earthquake.
6. Environmental Degradation: Drought conditions exacerbated by poor cropping patterns, overgrazing, the stripping of topsoil, poor conservation techniques, depletion of both surface and subsurface water supply.
7. Lack of Awareness and Information: Lack of knowledge about protective measures, safe locations, safe evacuation routes and procedures that can be accessed during a disaster can lead to community to experience impacts of the disaster since they don’t know how to reduce the effects.
8. War and Civil Strife: Includes competition for scarce resources, religious or ethnic intolerance and ideological differences e.g. the Rwandan massacre.

Phases of Disaster, victim’ response and roles of a Nurse

Disaster Action Phase

These are the steps in which a disaster will occur
There are three phases to any disaster. The actions on emergency personnel and others professional depend on which of the disaster is at hand.

Pre-impact Phase
Impact Phase
Post Impact Phase

PRE-IMPACT PHASE: This is an initial phase of disaster prior to the actual occurrence of warning is given at a sign of the first possible danger to the community. The earliest possible warning is crucial in preventing loss of life and minimizing damage. It is a period when emergency preparedness plan is made, first Aids Centre is opened and communication is very important, time for educating the community. The nurse’s role is to sensitize the community assist in making emergency shelters and prepare medical equipment.

IMPACT PHASE: Occurs when disaster has actually happened; it is time for enduring hardship or injury and trying to survive. It is an emergency period when the individual helps neighbours and families at a “scene”, a time of holding “on” until outside helps arrive. The phase may last longer depending on the type of disaster. This phase provides preliminary assessment of the nature extent and geographical area of the disaster. A period when needs of the victim in the community is assessed. The type and number of needed disaster health services is assessed, reports are given to centre for disease control and action taken. The role of a nurse is to assess health needs, provide physical and psycho-social support to mothers and children, given special shelters, injured persons are treated, coordinate search is made and re-union activities are made

POST IMPACT PHASE: This is a period of recovery from emergency phase and ends with return of normal community order and functioning. The phase may live longer and care must be given. The role of a nurse is to counsel, start rehabilitation, and sensitize the community for empowerment to start income generating activities

Classification of Disasters

Natural Disasters.
Human made Disasters

Natural Disasters

A natural disaster is a major adverse event or disaster resulting from natural processes of the Earth.

SUDDEN OCCURRENCE (MONOCAUSAL)
PROGRESSIVE OCCURRENCE (MULTICAUSAL)

SUDDEN OCCURANCE (MONOCAUSAL)	PROGRESSIVE OCCURRENCE (MULTICAUSAL)
STORM	LANDSLIDE
HEAT WAVE	DROUGHT
FREEZE	FLOODS
EARTHQUAKE	EPIDEMIC
VOLCANIC ERUPTION	PESTS

HUMAN MADE DISASTER

Human-made disasters are Emergency situations which are the results of deliberate human actions. They involve situations in which people suffers casualties, losses of basic services and means of livelihood

SUDDEN OCCURANCE (MONOCAUSAL)	PROGRESSIVE OCCURRENCE (MULTICAUSAL)
FIRE	WAR
EXPLOSION	ECONOMIC CRISIS
COLLISION
SHIPWRECK
STRUCTURAL COLLAPSE
ENVIRONMENTAL POLLUTION

Stages of emotional response

Victims of disaster usually go through 4 stages of emotional response.

Denial stage: Period when victims deny the magnitude of the problem or more likely may understand the problems but seems unaffected emotionally.
Strong Emotional Response: It is a stage when the person is aware but regards it as overwhelming and unbearable. Common reaction during this stage is fighting of feel, weeping, speaking with difficulty, trembling, and sadness. It is a period of counselling and reassurance.
Acceptance stage: It is the time when victims begin to accept either being handicapped with one leg.” I accept disaster, I try to make a decision for what to do next and develop hope.” The role of a Health worker is to help victim develop decision making, and take specific action.
Recovery stage: It is a stage of recovery from crisis reaction. Victims feel that they are back to normal and routines become important again and sense of wellbeing is restored.
Ability to make decision and carry out plans, returns victims, develops realistic memory.
The role of a nurse is to resettle the victims and discuss issues of empowerment if facilities are accessed.

Take your QUIZ about the above by clicking HERE.

Disaster Preparedness and Management Read More »

Introduction To Palliative Care

Palliative Care

Palliative care is an approach that improves the quality of life of patients and families facing the problem associated with life threating illness through the prevention and relief of suffering by means of early identification and assessment and treatment of pain and other problems which are physical , psychological and spiritual. WHO definition

Palliative care is the Active Total Care of patients with life limiting disease and their families, when the disease is no longer responsive to curative medicine.

Palliative care aims at achieving physical symptom relief but also extends far beyond it. It seeks to integrate physical, psychological, social and spiritual aspects of care so that patients may come to terms with their impending death as fully and constructively as they can.

History of Palliative Care

In 1960`s British Psychiatric John Hinton marked societal neglect and deficiency in the end of the life care. Hospices were sanctuaries provided by religious orders for the dying poor, providing food, clothes and shelter.

Dame Cicely Saunders an oxford trained nurse noted the trouble of dying and the need for improved pain control. She was a doctor, nurse social worker and a writer. She was the founder of the “Hospice Movement” in 1918. In 1967, Dame Cicely Saunders oversaw the building of the world’s first purpose built modern Hospice: St Christopher’s Hospice in London, England.

Saunders gave special care for the dying by providing expert pain and symptoms relief, with holistic care to meet the physical, social, psychological and spiritual needs of the patients and their families and friends.

Initially Hospice was reserved for those with incurable cancer. Now it has moved to include all “life limiting diseases” cancer, HIV/AIDS, Neurological disorders, Heart failure

At first, Hospices provided only inpatient care, isolated from mainstream care. Now there is inpatient Hospice care, home based care, hospital based teams and community outreach services.

Hospice is no longer a building it is a philosophy of care (Active Total Care of patients)

So now, What is Hospice Care, and  is it the same
or 
different from Palliative care.

Hospice Care

Hospice is an umbrella term for the carrying out of palliative care services and is usually a Centre where the team of professional and volunteers offer palliative services to people mainly with life limiting illness

There is an interface between hospice and palliative care. People often wonder the difference between hospice and palliative care

Therefore hospice is not the building

The word hospice origins from the hospes (Greek) and Hospitum (Latin) meaning hospitality

The major aim of hospice is to put life in the remaining days of a patient. It gives the possible quality of care for patient and their families from diagnosis of illness through critical episodes, end of life and bereavement support. Patients and their families are guests as they have choices and are encouraged to participate in discussions and make treatments and management choices.

Palliative care is the art and science of providing relief from illness – related suffering. Alleviation of suffering is needed for all patients who have curable and incurable illness. Hospice or end of life care can be used synonymous from palliative.

Hospice in Africa

Hospice has been established in the following countries: Zimbabwe, South Africa, Kenya, Uganda

In Uganda, Hospice services, were started in Nsambya Hospital in 1993 by Dr. Anne Merriman and since then organizations as well as hospitals have come up to offer palliative care services in Uganda such as Hospice Africa Uganda (HAU) and Mild may Uganda.
These service has further been extended to other parts of the Country by training specialist nurses and clinical officers who then deliver this care.

Seven (7) strategic objectives/Goals of Hospice

To provide High Quality African Palliative Care for cancer / HIV AIDS patients in Uganda;
To strengthen and maintain capacity of HAU(Hospice Africa Uganda) to produce oral liquid morphine;
To provide high quality palliative care training in Africa;
To build and strengthen capacity of other African countries to deliver palliative care;
To strengthen research, innovations, advocacy and networking for palliative care in Uganda and Africa;
To ensure effective and efficient governance at HAU(Hospice Africa Uganda)
To enhance financial efficiency and sustainability.

Need for palliative care

WHO estimates 9 million new cases of cancer each year (50% in developing countries).
More than 80% disease presents late and is often incurable.
Pain occurs in more than 66% of patients with advanced cancer
5 million HIV+ people live in sub–Saharan Africa
20-50% HIV patients can expect to suffer from severe

Philosophy/Roles of Palliative care

Affirms life.
Regards dying as a normal process.
Neither hastens nor postpones death.
Relieves pain and other distressing symptoms.
Integrates the psychological and spiritual aspects of care.
Offers support systems for patients to live as actively as possible until death
Offers support systems to help patients’ families cope during the patient’s illness and in their own bereavement.
Appropriate ethical considerations: Do good; do no harm, patient’s right to decide; and fairness.

Attributes of Palliative Care

Palliative care has a range of distinctive characteristics or attributes.

In palliative care, “attributes” refers to the characteristics, features, or qualities that are associated with or define palliative care. These attributes are the essential elements that make up the nature and scope of palliative care as a specialized form of medical care.

Here are the key attributes of palliative care:

Holistic approach: Palliative care takes a comprehensive approach to address the physical, emotional, psychological, social, and spiritual needs of the patient. It considers the person as a whole and not just the disease.
Pain and symptom management: Palliative care aims to alleviate pain, manage symptoms, and improve the patient’s comfort level. This involves using a combination of medications, therapies, and other interventions to control distressing symptoms.
Communication and coordination: Effective communication is crucial in palliative care. The care team works closely with the patient and their family to understand their preferences, goals, and values. They also facilitate coordination between different healthcare professionals to ensure seamless care delivery.
Patient-centered care: Palliative care respects the patient’s autonomy and individual preferences. It involves shared decision-making, where patients are actively involved in making choices about their care and treatment options.
Family support: Palliative care recognizes the impact of serious illness on the patient’s family members and caregivers. It offers emotional support, education, and guidance to help them cope with the challenges they may face.
Continuity of care: Palliative care is not limited to a specific location or time frame. It can be provided alongside curative treatments and is often delivered at different stages of the illness.
Advance care planning: Palliative care encourages patients to discuss and document their preferences for medical treatment and end-of-life care in advance. This helps ensure that their wishes are respected and followed.
Bereavement support: Palliative care extends its support to the family even after the patient’s death. Bereavement services help family members cope with grief and loss.
Interdisciplinary care team: Palliative care involves a team of healthcare professionals with various specialties, including doctors, nurses, social workers, chaplains, and other specialists as needed. This interdisciplinary approach ensures a comprehensive and well-coordinated care plan.
Dignity and respect: Palliative care emphasizes the importance of treating patients with respect, preserving their dignity, and providing compassionate care throughout their journey.

Essential components of palliative care

Palliative care has two components:

Pain and symptom control: Modern methods are used for pain relief, including oral morphine for severe pain, and symptom treatment and management.
Supportive care: The psychological, social, spiritual and cultural needs of the patient and the family, including bereavement care, are attended to.

Key aspects to palliative care

Focus on quality of life
Holistic approach
Multi disciplinary team (MDT)- doctor, nurse, physiotherapist, occupation therapist, social worker
Patient and family at center of care
Attention to details
Availability of essential drugs e.g. morphine
Peace, comfort and dignity of the patient and family.

Principles of Palliative Care

Patient centered: Palliative care revolves around the patient and their family. The focus is on maintaining hope with realistic goals, supporting the patient and their loved ones throughout different stages of the illness. Sustain hope with realistic goals in order to help patient and families cope in appropriate way through the different phase of the illness.
Appropriate ethical consideration: There are many ethical issues that arise in care of all patients. Seek to do good or do no harm, patients’ rights must be considered to decide fairly. Palliative care involves navigating various ethical issues. Remember to balance doing what’s best for the patient while respecting their rights and autonomy.
Continuum of treatment. This involves management of pain and other symptoms i.e. Palliative care begins from the time of diagnosis and extends beyond the patient’s passing. It includes pain and symptom management as well as providing bereavement care for the family after death. (bereavement
care).
Teamwork and partnership: Palliative care requires an interdisciplinary team to address the diverse needs of patients effectively. It is not easy to address all patients’ needs alone. An interdisciplinary team should be established to deal with all the problems. i.e. no single profession can address all issues that cause total pain. Team members share challenges facing the patient and plan effective management of the patient using their skill mix. A palliative care team includes:
1. Nurses
2. Doctor
3. Social workers
4. Religious leaders
5. Teachers
6. Community health providers > Others as appropriate.
Holistic care approach: Holistic care treats the patients as a whole person, not just as a medical case. This approach focuses not only on physical care, but also psychological (emotional), social and spiritual care. This psychological and emotional support and care should be available for the caregivers as well as the patient, family members, community volunteers, professional care and support workers (health workers, counselors, social workers), before, during and after periods of care giving.
Holistic care: this is care of whole person and is more than only drug and physical care

Components of holistic care

Physical care: This involves the assessment and management of pain and other physical symptoms. Its important because if physical symptoms are with them if they controlled other aspects will be different to carry.
Psychological care: Effective communication skills are crucial in caring for patients holistically. Providing emotional support, active listening, and compassionate understanding help patients cope with the emotional challenges they face.
Spiritual care: This is important to terminally ill and it includes allowing patients to express their spirituality, praying with them if they request for arranging for an appropriate leader to visit them.
Family support: The terminal phase of illness is often very difficult for patients’ family. Support therefore needs to be offered to the family. It includes spending time, listening and giving support to them.
Social care: This incorporates discussion of social and family issue e.g. This could include considering the well-being of young children who may become orphans and discussing financial matters that can impact the patient and their family.

Models of Palliative Care

Health facilities based: Palliative care is provided either in hospital at the outpatient department or in other clinics as designated by the in-charge. Health Centers IV and Ill with palliative care trained
health workers provide palliative care services using a facility palliative care team.
Health facility Out-reach programs: specialist palliative care health workers travel to other center to provide palliative care. Palliative care in this modal is provided by palliative care trained health workers. The team moves to the community to provide palliative care services closer to the community. Facility outreach programs are important in that they bring the services nearer to the
people. Hence patients do not have to walk long distances and a mass of people can be seen within their villages.
Roadside clinics/stopovers: This is a model of care that enables patients who live far away from health facilities to access palliative care. Health care providers plan with patients and their caregivers to
meet- in identified place along the route or on their way to an outreach. They make a stopover in an agreed place. The place location can be a trading Centre, under a tree, at a particular signpost or at a school.
Facility day care: This is when a day is set aside for the patient and their caretaker to spend time with other patients in at the facility. This facility could be a hospital, health Centre a hospice. This activity
enables recreation as well as socialization. Patients get to share their challenges encounter during the disease trajectory arid even counsel themselves. They interact as they enjoy lunch or tea, they also get an opportunity to see their nurses or doctors at the site and have they needs attended to.
Community day care: It is similar to facility day care except it is done within the community. Health care workers move to the community and spend the day with patients at a designated area in the community, it could be at the church, health Centre community hall or someone’s home.
Home based palliative care model: This means a delivery of a comprehensive package of care to the patient and the family at home. The package includes spiritual, psychological, pain and symptom management as well as support in activities of daily living. This model of care is best provided by a specialist palliative care team working in partnership with trained community health volunteers.

Services offered during home based palliative care:

Basic physical care such as recognition of symptoms; basic treatment and symptom management
Basic nursing care, such as positioning and mobility, bathing, wound cleaning, skin care, maintaining basic hygiene, oral care, taking medication.
Psychosocial support and counseling: being with the patient and family during a difficult time, providing listening and understanding, sharing a quiet moment, helping the family to access legal support.
Preventing transmission of infections such as HIV testing, disclosure, condoms, safe water
Provide spiritual support: listening to patients and families’ spiritual troubles and anxieties, praying with the patient, and preparation for death.
Household assistance- support patients with practical support such as washing clothes, cleaning, shopping
Providing health promotion: disease prevention such as HIV, TB
Training care takers in basic nursing skills and care.

Advantages and disadvantages of each model

Palliative Care Model	Advantages	Disadvantages
Health Facilities Based	– Accessible within health facilities	– May not reach patients in remote areas
	– Utilizes facility-based palliative care team	– Limited to patients who visit health centers
	– Expert care provided by trained health workers
Health Facility Outreach	– Brings care closer to the community	– Limited to specific outreach locations
Programs	– Allows for mass outreach and care provision	– Requires additional resources for travel
	– Utilizes trained palliative care specialists
Roadside Clinics/Stopovers	– Enables care for patients in remote areas	– Requires planning and coordination for stopovers
	– Convenient for patients and caregivers on the go	– May have limited medical resources during stopovers
Facility Day Care	– Provides recreation and socialization for patients	– Limited to designated facility and day
	– Allows patients to interact and share experiences	– Patients may require transportation to the facility
Community Day Care	– Brings care directly to the community	– Limited to specific designated areas
	– Enhances community involvement and support	– May lack necessary medical equipment and supplies
Home-Based Palliative Care	– Provides comprehensive care at home	– Requires a specialized palliative care team
Model	– Allows for spiritual, psychological, and symptom	– May be challenging in remote or underserved areas
	management in the comfort of the patient’s home	– Depends on the availability of trained volunteers
	– Supports the patient and family in daily activities

Challenges for implementing palliative care

Perception and recognition: many people still fear palliative care because they link it to death and many do not want to admit that they are dying. It is also common with health worker, policy makers
and others.
Policy development; sustainable, affordable and effective palliative care must be an integral of a country’s health system. To achieve this there must be coordination with all health sectors. Some
policies prohibit use of oral opioids, so advocacy for change is important
Education: health providers and community members need to be educated on diagnosis, classification and application of holistic approach. Training should be in medical/nursing schools
Drug availability: there are limited recourses including limited drug budget a palliative drugs are given priority because they are for symptoms relief. It is important for these drugs to be included in the
essential drug list.

Introduction To Palliative Care Read More »

Nephrotic and Nephritic syndromes

NEPHROTIC SYNDROME.

Nephrotic syndrome, or nephrosis, is a constellation of symptoms characterized by nephrotic range, massive proteinuria, edema, and hypoalbuminemia with or without hyperlipidemia.

MASSIVE Proteinuria >3.5g/24 hours Or spot urine protein: creatinine ratio >300 – 350 mg/mmol Hypoalbuminemia <25g/L,

Edema,(Generalized edema is called Anasarca)

And often: Hyperlipidemia/dyslipidemia (total cholesterol >10 mmol/L)

Additionally, the loss of immunoglobulins increases the risk of infection, while the loss of proteins that prevent clot formation puts patients at risk for blood clots.

Pathophysiology of Nephrotic Syndrome.

Nephrotic syndrome results from damage to the kidney’s glomeruli, the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine.

Damage to the glomeruli from diabetes or even prolonged hypertension causes the membrane to become porous, so that small proteins such as albumin pass through the kidneys into urine.

Glomerular Filtration Barrier Disruption: The renal glomerulus, responsible for filtering blood entering the kidney, consists of capillaries with small pores. In nephrotic syndrome, inflammation or hyalinization affects the glomeruli, allowing proteins, including albumin, antithrombin, and immunoglobulins, to pass through the normally restrictive cell membrane.
Proteinuria: Increased permeability results in the leakage of proteins into the urine. Albumin, a key protein for maintaining oncotic pressure in the blood, is lost in significant amounts.
Hypoalbuminemia: Loss of albumin in the urine reduces the oncotic pressure in the blood. Reduced oncotic pressure leads to the accumulation of fluid in the interstitial tissues, causing edema.
Hyperlipidemia: Hypoalbuminemia triggers compensatory mechanisms in the liver. The liver increases the synthesis of proteins such as alpha-2 macroglobulin and lipoproteins. Elevated lipoprotein levels contribute to hyperlipidemia associated with nephrotic syndrome.

Signs and symptoms

Manifestation of glomerular disease, characterized by nephrotic range proteinuria and a triad of clinical findings associated with large urinary losses of protein : hypoalbuminaemia , edema and hyperlipidemia

Weight Gain: Patients experience noticeable weight gain due to fluid retention. The retention of fluids, primarily as a result of massive proteinuria and reduced oncotic pressure, leads to increased body weight.

Facial Edema (Puffiness Around the Eyes): Swelling, particularly around the eyes, with a distinctive pattern. Generalized edema is called Anarsaca.

Morning Onset: The puffiness is most apparent in the morning and tends to subside throughout the day.
Location: Predominantly observed around the eyes.

Abdominal Swelling: Enlargement of the abdominal region. Associated with;

Pleural Effusion: Accumulation of fluid in the pleural cavity.
Labial or Scrotal Swelling: Swelling in the genital areas.

Edema of Intestinal Mucosa: Swelling of the intestinal mucosa leading to various gastrointestinal symptoms. Such as

Diarrhea: Resulting from edema affecting the intestinal lining.
Anorexia: Loss of appetite due to abdominal discomfort.
Poor Intestinal Absorption: Impaired absorption of nutrients, contributing to malnutrition.

Ankle/Leg Swelling: Edema affecting the lower extremities. Fluid accumulation in the ankles and legs due to altered fluid balance.

Behavioral Changes: Altered mood and behavior. Manifested as;

Irritability: Restlessness or frustration.
Easily Fatigued: Fatigue occurs more quickly than expected.
Lethargy: Persistent tiredness, indicating overall weakness.

Susceptibility to Infection: Increased vulnerability to infections. Loss of immunoglobulins in the urine, combined with potential immune system suppression from treatments like corticosteroids, increases the risk of infections.

Urine Alterations: Changes in urine characteristics. Such as;

Decreased Volume: Reduced urine output.
Frothy Urine: Presence of foam or bubbles in the urine, indicating significant proteinuria.
Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome. Hyponatremia also occurs with a low fractional sodium excretion.

Hyperlipidaemia: Hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins.

Anaemia (iron resistant microcytic hypochromic type) may be present due to transferrin loss.

Dyspnea may be present due to pleural effusion or due to diaphragmatic compression with ascites.

Other features: May have features of the underlying cause, such as the rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes.

Causes of Nephrotic Syndrome

Nephrotic syndrome has many causes and may either be the result of a glomerular disease that can be either limited to the kidney, called primary nephrotic syndrome (primary glomerulonephrosis), or a condition that affects the kidney and other parts of the body, called secondary nephrotic syndrome and other genetic causes.

Primary causes

Minimal change disease (MCD): is the most common cause of nephrotic syndrome in children. It owes its name to the fact that the nephrons appear normal when viewed with an optical microscope as the lesions are only visible using an electron microscope. Another symptom is a pronounced proteinuria.
Focal segmental glomerulosclerosis (FSGS): is the most common cause of nephrotic syndrome in adults. It is characterized by the appearance of tissue scarring in the glomeruli. The term focal is used as some of the glomeruli have scars, while others appear intact; the term segmental refers to the fact that only part of the glomerulus suffers the damage.
Membranous glomerulonephritis (MGN): The inflammation of the glomerular membrane causes increased leaking in the kidney. It is not clear why this condition develops in most people, although an auto-immune mechanism is suspected.
Membranoproliferative glomerulonephritis (MPGN): is the inflammation of the glomeruli along with the deposit of antibodies in their membranes, which makes filtration difficult.
Rapidly progressive glomerulonephritis (RPGN): (Usually presents as a nephritic syndrome) A patient’s glomeruli are present in a crescent moon shape. It is characterized clinically by a rapid decrease in the glomerular filtration rate (GFR) by at least 50% over a short period, usually from a few days to 3 months.

Secondary causes

Diabetic nephropathy: is a complication that occurs in some diabetics. Excess blood sugar accumulates in the kidney causing them to become inflamed and unable to carry out their normal function. This leads to the leakage of proteins into the urine.
Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among them the kidney, due to the deposit of immune complexes that are typical to this disease. The disease can also cause lupus nephritis.
Infections like; Syphilis: Kidney damage can occur during the secondary stage of this disease (between 2 and 8 weeks from onset). Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage them. HIV: the virus’s antigens provoke an obstruction in the glomerular capillary’s lumen that alters normal kidney function.
Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow and damages the kidney.
Cancer: as happens in myeloma, the invasion of the glomeruli by cancerous cells disturbs their normal functioning.
Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin, a component of the glomerular filtration barrier, is altered.
Drugs ( e.g. gold salts, penicillin, captopril): gold salts can cause a more or less important loss of proteins in urine as a consequence of metal accumulation. Penicillin is nephrotoxic in patients with kidney failure and captopril can aggravate proteinuria.

Diagnosis and Investigations

Initial Assessment:

Obtain a thorough medical history, including any acute or chronic conditions, family history of kidney disease, and a review of systems to identify symptoms such as edema, fatigue, and foamy urine.
Perform a physical examination focusing on signs of fluid overload, such as edema and ascites, as well as other systemic findings.

Laboratory Investigations:

Conduct urinalysis to detect the features of nephrotic syndrome: high levels of proteinuria.
Microscopic hematuria that may occasionally be present.
Biochemical tests to evaluate kidney function, including serum creatinine, blood urea nitrogen (BUN), electrolytes, albumin levels, and a lipid profile, as hyperlipidemia is often associated with nephrotic syndrome.
Perform a urine protein-to-creatinine ratio to quantify the degree of proteinuria.

Imaging Studies:

Ultrasound imaging: the kidneys may appear hyperechoic with a loss of corticomedullary differentiation.
If indicated, conduct an ultrasound of the entire abdomen to evaluate for complications such as venous thrombosis or to rule out other causes of proteinuria.

Immunological and Serological Testing:

Analyze auto-immune markers, including antinuclear antibodies (ANA), anti-streptolysin O titers (ASOT), complement components (such as C3), cryoglobulins, and perform serum electrophoresis to detect monoclonal gammopathy.

Kidney Biopsy:

If the initial tests are inconclusive or if it is important to determine the specific cause of nephrotic syndrome, Carry out a kidney biopsy. Histological examination can identify the type of glomerulonephritis or other glomerular pathology.

Additional Investigations:

Consider genetic testing if there is a suspicion of hereditary causes of nephrotic syndrome, especially in pediatric cases or when there is a family history of kidney disease.
Assess for secondary causes of nephrotic syndrome, which may include tests for infectious diseases (like hepatitis B and C, HIV), diabetes mellitus control (HbA1c), and evaluation for malignancies if clinically indicated.

Treatment of Nephrotic Syndrome

Aims of Management.

To reduce edema
To correct hypoalbuminemia
To lower blood pressure
To reduce proteinuria
To prevent complications such as infection, thrombosis, and malnutrition

Medical Management:

Diuretics: Loop diuretics, such as furosemide, are the mainstay of treatment for edema. Thiazide diuretics, such as hydrochlorothiazide, can be added if needed.
Albumin: Albumin infusions may be necessary to correct hypoalbuminemia and reduce edema. Not used because they are expensive.
ACE inhibitors or ARBs: ACE inhibitors, such as lisinopril, or ARBs, such as losartan, are used to lower blood pressure and reduce proteinuria.
Corticosteroids: Prednisone is the most commonly used corticosteroid for the treatment of nephrotic syndrome. Prednisone is started at a dose of 1-2 mg/kg/day and then tapered over several weeks. Lack of response to prednisolone therapy for 4 weeks is an Indication for renal biopsy.
Immunosuppressive drugs: Immunosuppressive drugs, such as cyclophosphamide, are used to treat patients who do not respond to corticosteroids.
Statins: Statins, such as atorvastatin, are used to lower cholesterol levels.
Antiplatelet agents: Antiplatelet agents, such as aspirin, are used to prevent thrombosis.
Nutritional support: Nutritional support, including a high-protein diet, is important to prevent malnutrition.
Vitamin D and calcium supplements: Vitamin D and calcium supplements may be necessary to prevent hypocalcemia.
Antibiotics: Antibiotics are used to treat infections.
Vaccinations: Vaccinations against pneumococcal pneumonia and influenza are recommended for patients with nephrotic syndrome.

Nursing Interventions for Nephrotic Syndrome:

Fluid Volume Excess:

Elevate the child’s legs and feet to promote fluid drainage.
Monitor for signs of fluid overload, such as edema, ascites, and pleural effusions.
Restrict fluid intake as prescribed by the physician.
Administer diuretics, such as furosemide (Lasix), as prescribed to promote fluid excretion.
Monitor intake and output strictly and maintain accurate fluid balance charts.
Weigh the child daily to monitor fluid status.

Ineffective Breathing Pattern:

Assess respiratory status regularly, including oxygen saturation, respiratory rate, and effort.
Position the child in a semi-Fowler’s position or over a table supported by pillows to improve lung expansion.
Provide oxygen therapy, if prescribed, to maintain adequate oxygenation.
Encourage the child to take slow, deep breaths and use relaxation techniques to reduce anxiety and improve breathing patterns.
Administer bronchodilators, if prescribed, to improve airflow and reduce wheezing.

Risk for Infection:

Monitor the child for signs of infection, such as fever, chills, and increased white blood cell count.
Administer antibiotics, as prescribed, to treat or prevent infections.
Practice strict hand hygiene and maintain aseptic technique when handling the child and performing procedures.
Keep the child’s skin clean and dry to prevent skin infections.
Monitor the child’s nutritional status and provide a diet rich in protein and vitamins to support the immune system.

Altered Nutrition: Less Than Body Requirements:

Provide small, frequent meals that are high in protein and calories to meet the child’s increased nutritional needs.
Offer a variety of foods to encourage the child to eat and prevent monotony.
Consult with a registered dietitian to develop a personalized nutrition plan that meets the child’s individual needs and preferences.
Supplement the child’s diet with nutritional supplements, as prescribed, to ensure adequate intake of essential nutrients.

Dietary Management of Nephrotic Syndrome:

Provide a balanced diet with adequate protein (1.5-2 g/kg) and calories.
Limit fat intake to less than 30% of total calories and avoid saturated fats.
Encourage the child to follow a “no added salt” diet to reduce fluid retention.
Discourage the consumption of high-sugar drinks and snacks to prevent weight gain and fluid overload.
Monitor the child’s weight regularly and adjust the diet as needed to maintain a healthy weight.

Complications:

Monitor for complications of nephrotic syndrome, such as ascites, pleural effusion, generalized edema, coagulation disorders, thrombosis, recurrent infections, renal failure, growth retardation, and calcium and vitamin D deficiency.
Provide appropriate interventions and treatments for any complications that arise.
Educate the child and family about the potential complications of nephrotic syndrome and the importance of regular follow-up care.

Complications of Nephrotic Syndrome:

Thromboembolic Disorders: Caused by decreased levels of antithrombin III, a protein that inhibits blood clotting. Antithrombin III is lost in the urine due to the increased permeability of the glomerular basement membrane. This can lead to the formation of blood clots in the veins (deep vein thrombosis) or arteries (pulmonary embolism).
Infections: Increased susceptibility to infections due to:

Loss of immunoglobulins and other protective proteins in the urine.
Decreased production of white blood cells.
Impaired immune cell function.
Common infections include pneumonia, cellulitis, and peritonitis.

Acute Kidney Failure: Caused by a decrease in blood volume (hypovolemia) due to fluid loss into the tissues (edema). Hypovolemia leads to decreased blood flow to the kidneys, which can damage the kidneys and cause acute kidney failure.
Pulmonary Edema: Caused by the loss of proteins from the blood plasma, which leads to a decrease in oncotic pressure. Decreased oncotic pressure allows fluid to leak out of the blood vessels into the lungs, causing pulmonary edema.
Hypothyroidism: Caused by the loss of thyroxine-binding globulin (TBG), a protein that binds to thyroid hormone and transports it in the blood. Decreased TBG levels lead to decreased levels of free thyroid hormone, which can cause hypothyroidism.
Vitamin D Deficiency: Caused by the loss of vitamin D-binding protein, a protein that binds to vitamin D and transports it in the blood. Decreased vitamin D-binding protein levels lead to decreased levels of free vitamin D, which can cause vitamin D deficiency.
Hypocalcemia: Caused by the loss of 25-hydroxycholecalciferol, the storage form of vitamin D. Vitamin D is necessary for the absorption of calcium from the intestines. Decreased vitamin D levels lead to decreased calcium absorption, which can cause hypocalcemia.
Microcytic Hypochromic Anemia: Caused by the loss of ferritin, a protein that stores iron in the body. Decreased ferritin levels lead to decreased iron stores, which can cause iron-deficiency anemia.
Protein Malnutrition: Caused by the loss of protein in the urine, which exceeds the amount of protein that is ingested. Protein malnutrition can lead to a number of health problems, including weakness, fatigue, and impaired immune function.
Growth Retardation: Can occur in children with nephrotic syndrome due to a number of factors, including:

Protein malnutrition.
Anorexia (reduced appetite).
Steroid therapy (which can suppress growth).

Cushing’s Syndrome: Can occur in patients with nephrotic syndrome who are treated with high doses of corticosteroids. Cushing’s syndrome is caused by the overproduction of the hormone cortisol, which can lead to a number of health problems, including weight gain, high blood pressure, and diabetes.

NEPHRITIC SYNDROME

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Differences between Nephrotic syndrome and Nephritic syndrome

Nephrotic and Nephritic syndromes Read More »

Glomerulonephritis

Glomerulonephritis (GN)

Glomerulonephritis (GN) refers to a group of kidney diseases characterized primarily by inflammation and damage to the glomeruli, the tiny filtering units within the kidneys.

Glomerulonephritis is an inflammatory condition of the kidneys characterized by increased permeability of the glomerular filtration barrier causing filtration of RBCs and proteins.

While the primary site of injury is the glomerulus, inflammation can sometimes extend to the small blood vessels (capillaries, arterioles) within the kidney.

Bilateral Involvement: GN usually affects both kidneys simultaneously due to the systemic nature of many underlying causes (e.g., immune responses, infections).

Review of Relevant Anatomy and Physiology: The Nephron and Glomerulus

Functional Unit: The nephron is the fundamental structural and functional unit of the kidney, responsible for filtering blood and producing urine. Each kidney contains approximately 1 million nephrons.

Nephron Structure:

Glomerular Capsule (Bowman’s Capsule): A cup-shaped structure at the closed end of the nephron tubule. It surrounds the glomerulus.
Glomerulus: A network (tuft) of tiny arterial capillaries enclosed within Bowman’s capsule. This is where blood filtration begins. Blood enters via the afferent arteriole and exits via the efferent arteriole.
Renal Tubule: Extending from Bowman’s capsule, this tubule is about 3 cm long and consists of three main parts:

Proximal Convoluted Tubule (PCT): Responsible for reabsorbing the majority of filtered water, electrolytes (Na+, K+, Cl-), glucose, amino acids, and bicarbonate.
Loop of Henle: A hairpin-shaped loop (with descending and ascending limbs) extending into the medulla. Crucial for establishing the concentration gradient in the kidney, allowing for urine concentration. Further water and electrolyte reabsorption occurs here.
Distal Convoluted Tubule (DCT): Involved in fine-tuning electrolyte and acid-base balance (e.g., reabsorbing Na+, Ca++; secreting K+, H+). Influenced by hormones like aldosterone and ADH (indirectly).

Collecting Duct: Several DCTs empty into a collecting duct. These ducts pass through the medulla, further adjusting water reabsorption (under ADH influence) and electrolyte balance before delivering urine to the renal pelvis.

Glomerular Filtration Membrane (GFM): The crucial barrier separating blood in the glomerular capillaries from the filtrate in Bowman’s space. It consists of three layers:

Endothelium: The inner lining of the capillaries, featuring fenestrations (pores) that allow passage of water and small solutes but block blood cells.
Glomerular Basement Membrane (GBM): A middle layer, acting as a key size-selective and charge-selective barrier, preventing larger proteins (like albumin) from passing through.
Epithelial Cells (Podocytes): The outer layer facing Bowman’s space. These cells have foot processes (pedicels) separated by filtration slits, covered by a slit diaphragm, providing a final barrier, particularly to medium-sized proteins.

Glomerular Filtration Rate (GFR): The volume of fluid filtered from the glomerular capillaries into Bowman’s capsule per unit of time.

Normal GFR: Approximately 125 mL/minute or 180 Liters/day.
Filtration Process: Water and small molecules (electrolytes, glucose, urea, amino acids) pass freely through the GFM. Blood cells and large proteins (like albumin) are normally retained in the blood.
Reabsorption: Most of the filtrate (over 99%) is reabsorbed back into the bloodstream by the renal tubules. Only about 1-1.5 mL of fluid per minute is typically excreted as urine.

Renal Blood Flow Regulation: The kidneys have intrinsic mechanisms (autoregulation) and are influenced by the autonomic nervous system (sympathetic and parasympathetic nerves) and hormones (like angiotensin II, prostaglandins) to maintain relatively stable blood flow and GFR despite fluctuations in systemic blood pressure.

Classification of Glomerulonephritis

GN can be classified in several ways, which often overlap:

Onset and Duration:

Acute Glomerulonephritis (AGN): Develops suddenly, often following an infection (like streptococcus). Onset can be days to weeks after the trigger. Typically presents with nephritic features (see below).
Chronic Glomerulonephritis (CGN): Develops gradually over several years, often silently in the early stages. It may follow an episode of acute GN or arise insidiously. It represents progressive scarring and loss of kidney function, eventually leading to Chronic Kidney Disease (CKD).
Rapidly Progressive Glomerulonephritis (RPGN): Characterized by rapid loss of kidney function (often a 50% decline in GFR within weeks to months). Histologically associated with crescent formation in Bowman’s space. This is a medical emergency.

Histological Pattern (Based on Kidney Biopsy):

Proliferative GN: Characterized by an increase in the number of cells within the glomerulus (e.g., endothelial, mesangial, epithelial cells, infiltrating inflammatory cells). Examples include:

IgA Nephropathy (most common primary GN worldwide)
Post-Infectious GN (e.g., post-streptococcal)
Membranoproliferative GN (MPGN)
Lupus Nephritis (certain classes)
RPGN (Crescentic GN)

Non-Proliferative GN: Characterized primarily by structural changes without significant hypercellularity. Examples include:

Minimal Change Disease (common cause of nephrotic syndrome in children)
Focal Segmental Glomerulosclerosis (FSGS)
Membranous Nephropathy (common cause of nephrotic syndrome in adults)

Clinical Manifestations (Signs and Symptoms)

Symptoms vary widely depending on the type, severity, and acuity of GN. Some patients may be asymptomatic initially.

Common Features (especially Nephritic pattern):

Hematuria: Blood in the urine. May be microscopic (detected only by test) or macroscopic (visible, often described as cola-colored, tea-colored, or smoky). RBC casts in urine sediment are highly suggestive of glomerular origin.
Proteinuria: Excess protein in the urine. Can range from mild to nephrotic range (>3.5g/day). May cause foamy urine.
Edema: Swelling, often starting around the eyes (periorbital edema, especially in the morning) and progressing to the legs (pedal edema), ankles, and potentially generalized (anasarca), including ascites (fluid in abdomen) and pleural effusions (fluid around lungs). Due to sodium/water retention and sometimes low albumin (in nephrotic syndrome).
Hypertension: New onset or worsening high blood pressure. Often related to fluid retention. Can be severe.
Oliguria/Anuria: Decreased urine output (<400-500 mL/day) or very low/no urine output. Indicates significant decline in GFR.
Dysuria: Painful urination (less common, but can occur).

Systemic Symptoms:

Fatigue/Malaise/Weakness: Due to anemia (from reduced erythropoietin production by failing kidneys or chronic inflammation), uremia, or the underlying disease.
Flank Pain: Aching pain in the back/sides over the kidney area (less common than in kidney stones or pyelonephritis, but can occur due to capsular stretching).
Fever & Chills: More common in acute, infection-related GN or systemic inflammatory conditions.
Headache: Often related to hypertension.
Gastrointestinal Disturbances: Nausea, vomiting, anorexia, abdominal pain (can be due to uremia or ascites).

Symptoms Related to Complications or Underlying Disease:

Shortness of Breath: Due to pulmonary edema (fluid in lungs) from fluid overload or heart failure.
Visual Disturbances: Blurred vision due to hypertensive retinopathy or retinal edema.
Symptoms of SLE, Vasculitis, etc.: Rash, joint pain, etc.
Chronic GN Symptoms: May be subtle initially, presenting later with signs of CKD like nocturia (frequent urination at night), bone pain/deformity (renal osteodystrophy), anemia, failure to thrive (in children).

Clinical Presentation of Glomerulonephritis

Nephritic Syndrome: Characterized by inflammation.

Key features include Hematuria (blood in urine, often cola-colored),
Hypertension,
Oliguria (reduced urine output),
Azotemia (increased BUN/Creatinine), and
mild to moderate Proteinuria.
Edema is common.
Post-streptococcal GN is a classic example.

Nephrotic Syndrome: Characterized by

heavy proteinuria (>3.5 g/day ),
Hypoalbuminemia (low blood albumin),
severe Edema, and
Hyperlipidemia (high cholesterol/triglycerides).
Minimal Change Disease and Membranous Nephropathy are classic examples.
(Note: Some GN types can present with mixed nephritic/nephrotic features or evolve from one pattern to another).

Etiology of Glomerulonephritis

Primary GN: The disease originates within the kidney itself, without evidence of a systemic disease trigger (though often immune-mediated). Examples: IgA Nephropathy, Minimal Change Disease, FSGS, Membranous Nephropathy.
Secondary GN: Occurs as a consequence of another underlying systemic disease or condition. Examples: Lupus Nephritis (from SLE), Diabetic Nephropathy, Vasculitis-associated GN (e.g., Wegener’s/GPA, Microscopic Polyangiitis), Anti-GBM Disease (Goodpasture’s Syndrome), GN related to infections (Hepatitis B/C, HIV, Endocarditis), certain cancers, or drug reactions.

Factors that can cause or increase the risk of developing GN include:

Infections:

Streptococcal Infections: Group A beta-hemolytic streptococci (causing strep throat or skin infections like impetigo) are a classic trigger for Post-Streptococcal Glomerulonephritis (PSGN), especially in children. Typically occurs 1-3 weeks after infection.
Other Bacterial Infections: Bacterial endocarditis, infected shunts.
Viral Infections: Hepatitis B, Hepatitis C, HIV.
Fungal/Parasitic Infections: Less common causes.

Immune Diseases (Autoimmune Conditions):

Systemic Lupus Erythematosus (SLE): Lupus nephritis is a common and serious complication.
Goodpasture’s Syndrome: Autoantibodies attack the GBM in kidneys and lungs.
IgA Nephropathy (Berger’s Disease): IgA antibody deposits in the glomeruli.
Vasculitis: Inflammation of blood vessels (e.g., Granulomatosis with Polyangiitis [Wegener’s], Microscopic Polyangiitis, Henoch-Schönlein Purpura [IgA Vasculitis]).

Systemic Diseases:

Diabetes Mellitus: Diabetic nephropathy is a leading cause of CKD, involving glomerular damage.
Hypertension: Can both cause kidney damage (nephrosclerosis) and be a consequence of GN. High BP exacerbates glomerular injury.

Hereditary Factors: Some forms of GN, like Alport syndrome or certain types of FSGS, have a genetic basis.

Other Factors:

Certain Cancers (e.g., lymphomas, solid tumors via paraneoplastic syndromes).
Exposure to certain drugs or toxins (e.g., NSAIDs, lithium, some antibiotics).
Idiopathic: In many cases, the specific cause remains unknown.

Pathophysiology of Glomerulonephritis

Acute glomerulonephritis following an infection and is thought to be as a result of immunological response.
The body responds to streptococci by producing antibodies which combine with bacterial antigens to form immune complexes.
As these antigen-antibody complexes travel through circulation, they get trapped in the glomeruli and activate an inflammatory response that results in injury to capillary walls.
As a result of the inflammation, the capillary lumen becomes smaller leading to renal insufficiency .
Injury to the capillaries increases permeability to large molecules-proteins hence can leak into urine.

Structural Damage:

Thickening of GFM: Basement membrane can thicken due to deposits or increased matrix production.
Cell Proliferation: Increased cell numbers within the glomerulus.
Podocyte Injury: Damage or effacement (flattening) of podocyte foot processes leads to increased protein leakage (proteinuria).
Breaks in GFM: Allows passage of red blood cells (hematuria) and larger amounts of protein.
Crescent Formation (in RPGN): Proliferation of cells (parietal epithelial cells, infiltrating macrophages) in Bowman’s space, compressing the glomerular tuft.

Functional Consequences:

Decreased GFR: Inflammation, scarring, and reduced filtration surface area impair the kidney’s ability to filter waste products.
Increased Permeability: Damage to the GFM leads to proteinuria and hematuria.

Progression:

Scarring (Glomerulosclerosis): Persistent injury leads to replacement of functional glomerular tissue with scar tissue.
Tubulointerstitial Fibrosis: Damage often extends to the surrounding tubules and interstitial tissue.
Loss of Nephrons: Progressive scarring leads to irreversible loss of nephrons and decline in kidney function (CKD).

Consequences of Reduced GFR and Damage:

Retention of Sodium and Water: Impaired filtration leads to fluid overload.
Hypertension: Caused by fluid overload and activation of the Renin-Angiotensin-Aldosterone System (RAAS).
Edema: Accumulation of excess fluid in interstitial spaces.
Azotemia/Uremia: Accumulation of nitrogenous waste products (urea, creatinine) in the blood.

Types of Glomerulonephritis

1. Diffuse proliferative glomerulonephritis

This is inflammation of the glomerulus affecting all glomeruli (diffuse) with an increased number of cells in them (proliferative). It usually follows transient infection especially beta hemolytic streptococci but other organisms can cause it.

It presents as acute nephritis with haematuria and proteinuria. Recovery is good in children and in adults 40% cases may develop hypertension and renal failure.

2. Focal/segmental proliferative glomerulonephritis:

This is inflammation of the glomerulus affecting some glomeruli (focal) with increased number of cells in them (proliferative). It is associated with systemic lupus erythematosus(SLE) or infective endocarditis. It presents also as an acute nephritis with haematuria and proteinuria and recovery is variable.

3. Membranous/mesangial proliferative/ membranoproliferative glomerulonephritis.

This is inflammation of the glomerulus with thickening of the glomerular basement membrane. It is due to infections like syphilis, malaria, hepatitis B, drugs like penicillamine, gold, diamorphine and tumors.

It presents as nephrotic syndrome with haematuria and proteinuria and recovery is variable but most case progress to chronic renal failure

4. Minimal change glomerulonephritis

This is inflammation of the glomerulus with no exact known cause. It presents as nephrotic syndrome with haematuria and proteinuria and recovery is good in children but recurrences are common in adults.

Glomerulonephritis can be acute if it occurs in days or weeks ie 1 – 3 weeks following a streptococcal infection or glomerular damage
Chronic glomerulonephritis occur over months or years and is characterized by progressive destruction (sclerosis) or glomeruli and gradual loss of renal function

Diagnostic Evaluation of Glomerulonephritis

A combination of history, physical exam, and laboratory/imaging tests are used. Kidney biopsy is often the definitive test.

History:

Recent infections (sore throat, skin infection).
Symptoms: onset, duration, nature (edema, urine color changes, fatigue, HTN).
Past medical history (diabetes, SLE, hypertension, prior kidney disease).
Family history of kidney disease.
Medication history (including NSAIDs, nephrotoxic drugs).

Physical Examination:

Blood pressure measurement.
Assessment for edema (periorbital, peripheral, ascites).
Signs of fluid overload (jugular venous distension, lung crackles/rales indicating pulmonary edema).
Skin examination (rashes, signs of infection like impetigo, signs of vasculitis).
Observation for pallor (anemia), signs of uremia (e.g., uremic frost – rare now).
Assessment of visual acuity and fundoscopy (for hypertensive changes).

Urinalysis (Crucial first step):

Dipstick: Detects protein, blood, leukocytes, nitrites.
Microscopy: Quantifies RBCs, WBCs. Crucially looks for casts (cylindrical structures formed in tubules):

RBC Casts: Strongly suggest glomerular bleeding (hallmark of nephritic syndrome).
WBC Casts: Indicate inflammation (can be seen in GN, pyelonephritis, interstitial nephritis).
Granular Casts/Waxy Casts: Indicate tubular damage/stasis, often seen in more chronic disease.

Urine Protein Quantification: 24-hour urine collection or spot urine protein-to-creatinine ratio (UPCR) or albumin-to-creatinine ratio (UACR) to measure protein loss accurately.
Urine pH, specific gravity.

Blood Tests:

Renal Function Tests: Blood Urea Nitrogen (BUN) and Serum Creatinine (elevated levels indicate reduced GFR). Estimated GFR (eGFR) calculation.
Electrolytes: Sodium, Potassium (can be elevated, especially with oliguria), Chloride, Bicarbonate (may be low – metabolic acidosis). Calcium, Phosphorus (abnormalities common in CKD).
Complete Blood Count (CBC): Assess for anemia (normocytic, normochromic often seen in CKD), signs of infection.
Serum Albumin: Low levels (hypoalbuminemia) are characteristic of nephrotic syndrome.
Lipid Profile: Cholesterol and triglycerides are often elevated in nephrotic syndrome.
Inflammatory Markers: Erythrocyte Sedimentation Rate (ESR) or C-Reactive Protein (CRP) may be elevated.
Serological Tests (to identify cause):

Complement Levels (C3, C4): Low C3 is typical in post-streptococcal GN and some forms of MPGN/lupus nephritis. C4 may also be low in lupus.
Anti-Streptolysin O (ASO) Titre: Elevated titres suggest recent streptococcal infection (useful for PSGN diagnosis). Anti-DNase B is another marker for strep.
Antinuclear Antibody (ANA): Screening test for SLE.
Anti-dsDNA Antibody: Specific for SLE.
Anti-Glomerular Basement Membrane (Anti-GBM) Antibody: For Goodpasture’s syndrome.
Antineutrophil Cytoplasmic Antibodies (ANCA – c-ANCA, p-ANCA): For ANCA-associated vasculitis (GPA, MPA).
Hepatitis B/C Serology, HIV Test: To rule out infection-associated GN.

Imaging Studies:

Renal Ultrasound (USG): Assesses kidney size (often normal/enlarged in acute GN, small/scarred in chronic GN), echogenicity, rules out obstruction, and guides biopsy.
Chest X-ray: May show signs of fluid overload (pulmonary edema, pleural effusions, cardiomegaly).
Intravenous Pyelogram (IVP): Less commonly used now due to contrast risks and availability of other imaging; previously used to visualize urinary tract structures. CT or MRI may sometimes be used.

Kidney Biopsy:

Gold Standard: Provides a definitive diagnosis by allowing histological examination of kidney tissue (glomeruli, tubules, interstitium, vessels).
Information Gained: Identifies the specific type of GN, assesses the severity of inflammation/scarring (activity and chronicity), guides treatment decisions, and helps determine prognosis. Performed using light microscopy, immunofluorescence (to detect immune deposits like IgG, IgA, IgM, C3, C1q), and electron microscopy (for ultrastructural details like deposit location, podocyte changes).

Management of Glomerulonephritis

Aims of Management

Treatment goals depend on the type, severity, and underlying cause of GN.

General goals include:

preserving kidney function,
managing symptoms,
treating the underlying cause if possible, and
preventing complications.

General Supportive Measures:

Blood Pressure Control: Crucial for slowing progression. Often requires multiple medications. ACE inhibitors (ACEi) or Angiotensin II Receptor Blockers (ARBs) are often preferred as they can also reduce proteinuria. Target BP is usually <130/80 mmHg, potentially lower if proteinuria is significant.

Maintain Healthy Weight: Through appropriate diet and exercise (as tolerated).

Fluid Management:

Sodium and Water Restriction: To control edema and hypertension. Fluid intake may be limited based on urine output and fluid status.
Diuretics: Loop diuretics (e.g., furosemide) are commonly used to manage fluid overload and edema. Thiazides may be added if needed.

Dietary Modifications:

Protein Restriction: May be recommended in CKD to reduce workload on kidneys, but needs careful balancing to avoid malnutrition. Limit usually guided by GFR level. Less restriction or even normal intake may be needed in nephrotic syndrome to compensate for losses, requires careful monitoring.
Potassium, Phosphorus, Magnesium Restriction: Necessary if levels are elevated, common in advanced CKD. Requires avoiding certain foods and potentially using phosphate binders.
Calcium Supplements: May be needed if dietary intake is low or due to CKD mineral bone disease, often alongside Vitamin D analogues.

Specific Treatments (Based on GN type/cause):

Treating Underlying Infections: Antibiotics for bacterial infections (e.g., penicillin for post-streptococcal GN prevention in outbreaks or treating active infection; treatment for endocarditis). Antivirals for Hepatitis B/C or HIV.

Plasma Exchange (Plasmapheresis): Removes harmful antibodies from the blood. Used in conditions like Anti-GBM disease and severe ANCA-associated vasculitis.

Immunosuppression: Used for many primary immune-mediated GN and secondary forms like lupus nephritis or vasculitis. Aims to reduce inflammation and harmful immune responses.

Corticosteroids (e.g., Prednisone): Mainstay for many types.
Cytotoxic Agents (e.g., Cyclophosphamide, Mycophenolate Mofetil [MMF], Azathioprine): Used for more severe or resistant cases.
Calcineurin Inhibitors (e.g., Tacrolimus, Cyclosporine): Used for some types like Minimal Change, FSGS, Membranous.
Biologic Agents (e.g., Rituximab – targets B cells): Increasingly used for ANCA vasculitis, lupus nephritis, some other types.
(Immunosuppression carries risks of infection, malignancy, and other side effects, requiring careful monitoring).

Management of Complications:

Dialysis (Hemodialysis or Peritoneal Dialysis): Required for acute kidney injury with severe complications (fluid overload, hyperkalemia, acidosis, uremia) or for End-Stage Renal Disease (ESRD) when GFR is very low (<15 mL/min).
Anemia Management: Erythropoiesis-stimulating agents (ESAs) and iron supplementation.
Mineral and Bone Disorder Management: Phosphate binders, Vitamin D analogues, calcimimetics.
Hyperlipidemia Management: Statins may be used, especially in nephrotic syndrome.

Lifestyle Changes & Patient Education:

Adherence to medications, diet, and fluid restrictions.
Regular monitoring of BP, weight, and symptoms.
Smoking cessation.
Avoidance of nephrotoxic substances (e.g., NSAIDs, certain contrast dyes).
Understanding the disease, treatment plan, and potential complications.

Physiotherapy and Supportive Care:

Endurance Exercise: As tolerated (walking, swimming, cycling) can improve cardiovascular health, circulation, and well-being. Helps kidneys discharge waste and toxins by improving overall circulation.
Breathing Exercises: Pursed-lip breathing and diaphragmatic breathing can help manage shortness of breath associated with fluid overload or anxiety.
Edema Management: Elevation of edematous limbs, gentle range-of-motion exercises. Lymphatic massage may be considered for persistent edema, but primary treatment is addressing the underlying fluid overload medically.
Energy Conservation Techniques: Pacing activities, rest periods, especially if fatigued due to anemia or uremia.

Nursing Management

Goals of Nursing Care:

Maintain fluid and electrolyte balance.
Achieve and maintain target blood pressure.
Alleviate pain and discomfort.
Maintain effective breathing pattern and gas exchange.
Prevent skin breakdown.
Prevent infection.
Maintain adequate nutritional status.
Patient verbalizes understanding of disease and treatment plan.
Patient copes effectively with diagnosis and lifestyle changes.

Assessment:

Vital Signs: Frequent BP monitoring, heart rate, respiratory rate, temperature.
Fluid Balance: Strict intake and output monitoring, daily weights (most sensitive indicator of fluid status), assessment for edema (location, severity, pitting), jugular venous distension, lung sounds.
Symptoms: Assess for changes in urine (color, amount, foaminess), fatigue, shortness of breath, pain, nausea/vomiting.
Skin Integrity: Assess edematous areas for breakdown.
Neurological Status: Assess for headache, visual changes, confusion (signs of severe HTN or uremia).
Psychosocial Assessment: Coping mechanisms, anxiety, knowledge about the disease.
Monitor Lab Results: BUN, Creatinine, electrolytes, CBC, albumin, etc.

Nursing Diagnoses :

Excess Fluid Volume related to compromised regulatory mechanisms (renal failure) and sodium/water retention as evidenced by edema, weight gain, hypertension, abnormal lung sounds, decreased urine output.
Acute Pain related to inflammation of the renal cortex/capsular distension as evidenced by patient report of flank pain, facial grimacing.
Ineffective Breathing Pattern or Impaired Gas Exchange related to fluid overload (pulmonary edema) as evidenced by dyspnea, tachypnea, abnormal breath sounds, low oxygen saturation.
Risk for Impaired Skin Integrity related to edema.
Decreased Activity tolerance related to fatigue (anemia, uremia) and fluid overload.
Inadequate nutritional intake related to anorexia, nausea, dietary restrictions.
Risk for Infection related to altered immune status or immunosuppressive therapy.
Disrupted Body Image related to edema, presence of dialysis access, or chronic illness.
Excessive anxiety related to diagnosis, prognosis, and treatment complexity.
Deficient Knowledge related to disease process, dietary restrictions, medications, and self-care management.

Interventions:

Fluid Management: Administer diuretics as ordered, enforce fluid/sodium restrictions accurately, monitor I&O and daily weights meticulously, elevate edematous extremities, assist with frequent position changes to mobilize fluid and prevent skin breakdown.
Blood Pressure Management: Administer antihypertensives as ordered, monitor BP closely (before/after meds, postural checks if indicated).
Pain Management: Assess pain thoroughly (onset, location, quality, severity), provide comfort measures (positioning, quiet environment), administer analgesics as ordered (use caution with NSAIDs), explore relaxation techniques/diversion therapy.
Respiratory Support: Elevate head of bed (Semi-Fowler’s or High-Fowler’s position) to ease breathing, monitor respiratory status (rate, depth, effort, O2 saturation), administer oxygen as needed, encourage deep breathing/coughing exercises (if appropriate, not overly strenuous).
Nutritional Support: Collaborate with dietitian, provide prescribed diet, monitor intake, manage nausea/vomiting (antiemetics as ordered), provide oral care.
Skin Care: Gentle cleansing, moisturizing, use pressure-relieving surfaces if bed-bound, handle edematous skin carefully.
Activity Management: Encourage rest periods, assist with ADLs as needed, gradually increase activity as tolerated, plan activities to conserve energy.
Infection Prevention: Monitor for signs of infection (fever, increased WBC, site-specific signs), use aseptic technique, educate patient on hand hygiene and avoiding sick contacts (especially if immunosuppressed).
Medication Administration: Administer all medications accurately and on time (diuretics, antihypertensives, immunosuppressants, antibiotics, phosphate binders, etc.), monitor for therapeutic effects and side effects. Administer albumin infusions as ordered (helps shift fluid from interstitial space to intravascular space, often followed by diuretics).
Psychosocial Support: Provide emotional support, encourage verbalization of feelings, involve family, provide clear explanations, refer to support groups or counseling if needed.
Patient Education: Teach about the disease, medications (purpose, dose, side effects), dietary/fluid restrictions, monitoring (BP, weight, symptoms), when to seek medical attention, importance of follow-up.
Preparation for Procedures: Educate and prepare patient for kidney biopsy, dialysis initiation if necessary.

Complications of Glomerulonephritis

GN can lead to various acute and chronic complications:

Acute Kidney Injury (AKI) / Acute Renal Failure: Rapid decline in kidney function.
Chronic Kidney Disease (CKD): Progressive, irreversible loss of kidney function over time.
End-Stage Renal Disease (ESRD): Kidney function fails completely, requiring dialysis or transplantation.
Nephrotic Syndrome: (If not the primary presentation).
Hypertension: Often difficult to control, increases cardiovascular risk.
Electrolyte Imbalances: Hyperkalemia (high potassium – dangerous!), hyperphosphatemia, hypocalcemia, metabolic acidosis.
Anemia: Due to decreased erythropoietin production.
Increased Susceptibility to Infections: Due to the disease itself or immunosuppressive therapy.
Cardiovascular Disease: Increased risk of heart attack, stroke.
Renal Osteodystrophy: Bone disease related to CKD.
Hypertensive Encephalopathy: Neurological symptoms due to severely elevated blood pressure (headache, confusion, seizures).
Fluid Overload: Leading to:

Pulmonary Edema: Fluid accumulation in the lungs, causing severe shortness of breath.
Congestive Heart Failure (CHF): Heart struggles to cope with excess fluid volume.

Glomerulonephritis Read More »

Renal Failure

RENAL FAILURE (Acute and Chronic)

Renal failure refers to reduction in renal/kidney function.

Renal failure, also known as kidney failure, describes a situation where the kidneys lose their ability to function adequately.

This means they cannot effectively filter waste products from the blood, regulate electrolytes and fluids, or perform their essential endocrine functions.

The term “renal insufficiency” was formerly used but “kidney failure” is now more common, especially when function is significantly impaired.

The fundamental issue in renal failure is a reduction in the kidney’s excretory and regulatory functions.

Excretory Function Loss: Inability to remove metabolic wastes (like urea, creatinine, uric acid) and excess electrolytes (like potassium, phosphate) from the blood and excrete them in urine.

Regulatory Function Loss: Impaired ability to maintain:

Fluid balance (leading to overload or dehydration).
Electrolyte balance (e.g., potassium, sodium, calcium, phosphate).
Acid-base balance (often leading to metabolic acidosis).
Blood pressure control (through renin-angiotensin system and fluid balance).

Consequences of Kidney Function Failure:

Waste Product Accumulation: Toxic metabolic byproducts (urea, creatinine, nitrogenous wastes) build up in the blood – a condition known as azotemia. If symptoms develop due to azotemia, it’s called uremia.

Fluid Imbalance: Kidneys struggle to excrete excess fluid, leading to fluid overload, edema (swelling in legs, ankles, feet, lungs), and hypertension.

Electrolyte Disturbances:

Hyperkalemia: High potassium levels (critical, can cause fatal heart rhythm problems).
Hyperphosphatemia/Hypocalcemia: High phosphate and low calcium (due to decreased excretion of phosphate and impaired Vitamin D activation). This leads to bone disease.
Sodium Imbalance: Can be high, low, or normal depending on fluid status and intake/output.

Acid-Base Disturbances: Kidneys cannot excrete metabolic acids or regenerate bicarbonate effectively, leading to metabolic acidosis.

Endocrine Disruption:

Decreased production of erythropoietin (EPO), leading to anemia.
Impaired activation of Vitamin D, contributing to hypocalcemia and bone disease (renal osteodystrophy).
Altered insulin metabolism (kidneys help degrade insulin; failure can lead to longer insulin half-life).

Types of Renal Failure:

Acute Renal Failure (ARF) / Acute Kidney Injury (AKI): Characterized by a sudden onset (hours to days) of kidney dysfunction, often reversible if the underlying cause is treated promptly.
Chronic Renal Failure (CRF) / Chronic Kidney Disease (CKD): Characterized by a gradual, progressive, and irreversible loss of kidney function occurring over months to years.

ACUTE RENAL FAILURE (ARF) / ACUTE KIDNEY INJURY (AKI)

Acute Renal Failure is the rapid decline in the kidney’s ability to clear the blood of toxic substances e.g poison, drugs and antibodies that react against the kidneys leading to accumulation of metabolic waste products e.g. urea in blood.

AKI is the abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes. It’s characterized by a sudden and often complete loss of the kidneys’ ability to remove waste, occurring over hours, days, or sometimes weeks. While potentially reversible, it carries significant morbidity and mortality.

A healthy adult eating a normal diet needs a minimum daily urine output of approximately 400 ml to excrete the body’s waste products through the kidneys. An amount lower than this indicates a decreased GFR.

Key Markers/Characteristics: AKI is usually marked by:

Decreased Glomerular Filtration Rate (GFR): A rapid decline in the rate at which the kidneys filter blood.
Increased Serum Creatinine and BUN: Azotemia develops quickly as waste products accumulate. Creatinine rise is a key diagnostic indicator.
Oliguria: Urine output less than 400 ml per day (or <0.5 ml/kg/hr). However, AKI can also be non-oliguric, where urine output is normal or even high, but the kidneys are still not filtering waste effectively. Anuria (urine output <100 ml/day) can also occur.
Hyperkalemia: Potentially life-threatening elevation of potassium levels due to impaired excretion. (Normal K+ range approx. 3.6 to 5.2 mmol/L).
Sodium and Water Retention: Leading to edema and hypertension.
Metabolic Acidosis: Due to impaired acid excretion.

Risk Factors for AKI:

Hospitalization: Especially ICU admission.
Advanced Age: Reduced baseline GFR, more comorbidities.
Pre-existing Chronic Kidney Disease (CKD): Reduced renal reserve.
Diabetes Mellitus: Underlying nephropathy, vascular disease.
Hypertension: Underlying vascular disease.
Heart Failure: Reduced cardiac output, cardiorenal syndrome.
Liver Disease: Hepatorenal syndrome, altered hemodynamics.
Peripheral Artery Disease: Marker of systemic atherosclerosis, may involve renal arteries.
Sepsis: Hypotension, inflammation, direct kidney effects.
Volume Depletion (Dehydration): Common precipitant.
Exposure to Nephrotoxins: Contrast dye, certain antibiotics (aminoglycosides, vancomycin), NSAIDs.
Major Surgery: Especially cardiac or vascular surgery (risk of hypotension, emboli).

Pathophysiology of Acute Renal Failure/Acute Kidney Failure

Although the pathogenesis of Acute Renal Failure and oliguria is not always known, many times there is a specific underlying problem.

There are underlying problems that cause the development of Acute Renal Failure such as hypovolemia, hypotension, reduced cardiac output and failure, and obstruction of the kidney.

Pathophysiology Summary (Simplified Flow):
Initial Insult (Prerenal, Intrarenal, Postrenal) → Decreased Renal Perfusion / Direct Tubular/Glomerular Damage / Obstruction → Decreased GFR → Activation of RAAS & Sympathetic Nervous System (attempt to preserve BP/volume) → Renal Vasoconstriction → Further Decrease in Renal Blood Flow & GFR → Tubular Cell Injury/Dysfunction (impaired reabsorption/secretion) → Sodium & Fluid Retention (Edema, Hypertension) → Decreased Waste Excretion (Azotemia) → Decreased Acid Excretion (Metabolic Acidosis) → Decreased Potassium Excretion (Hyperkalemia) → Oliguria / AKI Manifestations

Etiology of Acute Renal Failure

A. Prerenal Acute Renal Failure:

This category involves conditions that reduce blood supply to the kidneys, leading to ischemia (reduced blood flow) and damage to the kidney tissue. The kidneys are highly sensitive to blood flow reduction, as they require a constant supply of oxygen and nutrients to function properly.

1. Hypovolemia (Low Blood Volume):

Causes:

Hemorrhage: Significant blood loss due to trauma, surgery, or internal bleeding.
Anemia: Severe anemia reduces the oxygen-carrying capacity of the blood, leading to insufficient oxygen delivery to the kidneys.
Asphyxia: Suffocation or airway obstruction reduces oxygen intake, compromising oxygen supply to the kidneys.
Burns: Extensive burns lead to fluid loss and decreased blood volume.
Dehydration: Inadequate fluid intake or excessive fluid loss due to sweating, vomiting, or diarrhea.
Gastrointestinal Fluid Loss: Vomiting, diarrhea, surgical drainage, and malabsorption can deplete blood volume.
Renal Fluid Loss:Osmotic Diuresis: Conditions like diabetes mellitus and hypoadrenalism lead to excessive urine production, depleting blood volume.
Sequestration in High Vascular Areas: Conditions like pancreatitis and trauma can cause fluid accumulation in certain areas, leading to decreased blood volume circulating to the kidneys.

2. Low Cardiac Output:

Causes:

Myocardial Diseases: Heart muscle diseases like heart failure, cardiomyopathy, and myocardial infarction can reduce the heart’s ability to pump blood effectively.
Valvular Diseases: Diseases of the heart valves, like stenosis or regurgitation, can obstruct blood flow and reduce cardiac output.
Pericardial Diseases: Pericarditis, pericardial effusion, and cardiac tamponade can restrict heart function, leading to reduced cardiac output.
Arrhythmias: Irregular heartbeats can compromise the efficiency of blood pumping.
Pulmonary Hypertension: High blood pressure in the lungs increases the workload on the heart, potentially leading to reduced cardiac output.
Massive Pulmonary Embolism: Blood clots in the lungs can block blood flow, reducing cardiac output.
Septic Shock: Severe infection can lead to widespread vasodilation and reduced blood pressure, compromising blood flow to the kidneys.

B. Intrarenal/Intrinsic Renal Causes:

This category involves direct damage to the kidney tissue itself, often triggered by inflammatory or immunological responses.

1. Toxins:

Nephrotoxic Drugs:

Aminoglycosides: Antibiotics like streptomycin and gentamicin can cause direct damage to kidney tubules.
Rifampicin: An anti-tuberculosis drug that can be nephrotoxic.
Tetracycline: An antibiotic that can cause kidney damage, particularly in children.
Other Nephrotoxins: Contrast dyes, certain chemotherapy drugs, and NSAIDs (non-steroidal anti-inflammatory drugs) can also damage the kidneys.

Heavy Metals: Exposure to heavy metals like phenol, carbon tetrachloride, and chlorates can cause significant kidney damage.

Endogenous Toxins:

Hemolysis: Destruction of red blood cells, often due to Rh incompatibility, releases toxic substances that can damage the kidneys.
Uric Acid Oxalates: High levels of uric acid and oxalates in the blood can form crystals that damage kidney tissue.

2. Diseases of the Glomeruli:

Glomerulonephritis: Inflammation of the glomeruli, the tiny filtering units in the kidneys. This can be caused by infections, autoimmune diseases, or other factors.
Pyelonephritis: Infection of the kidneys and the pelvis of the kidneys.

3. Acute Tubular Necrosis:

Causes: Damage to the tubules, the functional units of the kidneys, can be caused by toxins, ischemia, or other factors. This leads to impaired reabsorption and secretion of fluids and electrolytes.

4. Vasculitis: Inflammation of the blood vessels in the kidneys can damage the filtering units and reduce blood flow.

C. Post-Renal Causes:

This category involves obstruction of the urinary outflow tract, preventing urine from being drained from the kidneys.

Causes:

Tumors: Tumors in the bladder, prostate, or other parts of the urinary tract can block urine flow.
Stones: Kidney stones or bladder stones can obstruct the flow of urine.
Edema: Swelling in the urinary tract, often due to infection or inflammation, can obstruct urine flow.
Prostatic Hyperplasia: Enlargement of the prostate gland can compress the urethra, blocking urine flow.
Other Obstructions: Urethral strictures, congenital abnormalities, and trauma can also cause urinary outflow obstruction.

Phases/Stages of Acute Renal Failure

There are four phases of Acute Renal Failure when Initiation phase is included, otherwise they are 3 stages that begin with Oliguria

Initiation(Onset)or Asymptomatic Phase: The initiation period begins with the initial insult, and ends when oliguria develops. Period from the initial insult until signs/symptoms become apparent. Kidney injury is evolving. Early intervention here can prevent progression. Lasts hours to days. In the early stages of renal failure, often referred to as the asymptomatic phase, the kidneys start to lose their function, but individuals may not experience any noticeable symptoms. This phase can last for months or even years, and kidney damage may progress gradually without apparent signs.
Oliguric Phase/ Oliguria. This stage is characterized by reduced urine output of <400mls/day. This phase lasts 1-2 weeks. The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by kidneys. Other symptoms that may manifest during this phase include fatigue, fluid retention leading to edema (swelling), electrolyte imbalances, high blood pressure, and a buildup of waste products in the blood. Significant fall in GFR and urine output (<400 mL/day). Accumulation of fluid, electrolytes (K+, Phos), and waste products (BUN, Cr). Metabolic acidosis worsens. Complications are most likely during this phase.
Diuretic Phase/ Diuresis. Urine output increases to as much as 4000 mL/day but no waste products, at the end of this stage you may begin to see improvement. The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. GFR starts to rise, BUN/Cr start to fall (lagging behind urine output). Patient is at risk for dehydration and electrolyte losses (hypokalemia, hyponatremia). Lasts approximately 1-3 weeks.
Recovery. The recovery period signals the improvement of renal function and may take 3 to 12 months. If it is insufficient, it develops to Chronic renal failure. GFR increases, and tubular function normalizes. BUN and creatinine levels return towards baseline. Some patients recover fully, while others may have residual kidney damage or progress to CKD.

However, it’s important to note that not all cases of renal failure have a recovery phase, especially in chronic kidney disease (CKD), where kidney damage tends to be irreversible.

● End-Stage Renal Disease (ESRD): If renal failure progresses to a point where the kidneys are functioning at less than 10-15% of their normal capacity, it is referred to as end-stage renal disease (ESRD). At this stage, kidney function is severely compromised, and individuals require renal replacement therapies such as dialysis or kidney transplantation to sustain life.

Clinical features of Acute Renal Failure

Acute renal failure (ARF) is a sudden decline in kidney function, leading to a buildup of waste products in the blood and a disruption in fluid and electrolyte balance.

1. Reduced Urine Output (Oliguria): Occurs within 1-3 days, a rapid decrease in urine output occurs, often accompanied by a significant rise in blood urea nitrogen (BUN) and creatinine levels.

Duration: This phase, known as the oliguric phase, can persist for 7-20 days, depending on the severity and underlying cause of ARF.
Mechanism: The kidneys are unable to effectively filter waste products and excess fluids from the bloodstream, leading to their accumulation.

2. Electrolyte Imbalance:

Hyperkalemia: Increased potassium levels in the blood due to the kidneys’ inability to excrete potassium efficiently. This can lead to potentially life-threatening cardiac arrhythmias.
Other imbalances: Sodium, calcium, and phosphate levels may also be affected, contributing to various symptoms.

3. Fluid Imbalance:

Generalized Edema: Fluid retention due to decreased urine output can cause swelling in the legs, ankles, feet, and even the lungs (pulmonary edema).

4. Gastrointestinal Symptoms:

Decreased Appetite: Nausea and vomiting are common due to the accumulation of toxins in the body and electrolyte disturbances.

5. Lethargy and Fatigue:

Weakness and drowsiness: The body’s energy levels are depleted due to impaired kidney function and electrolyte imbalances.

6. Central Nervous System (CNS) Symptoms:

Drowsiness, headache, confusion: Accumulation of toxins in the bloodstream can affect brain function.
Muscle twitching, seizures/convulsions: Severe electrolyte imbalances, particularly hyperkalemia, can lead to seizures.

7. Pallor:

Pale skin: Anemia, a common complication of ARF, can cause pallor due to the kidneys’ inability to produce erythropoietin, a hormone essential for red blood cell production.

8. Pulmonary Edema:

Dyspnea (shortness of breath): Fluid accumulation in the lungs can make breathing difficult.

9. Dehydration:

Dryness of skin and mucous membranes: Reduced fluid intake and inability to excrete waste products lead to dehydration, manifesting as dry skin and mucous membranes.

10. Cardiovascular Signs:

Congestive heart failure: Fluid overload and electrolyte disturbances can strain the heart, leading to heart failure.
Severe hypertension: Decreased kidney function can contribute to high blood pressure, potentially leading to complications such as stroke.

Investigations/Diagnostic Findings

Urine

Volume: Usually less than 100 mL/24 hours (anuric phase) or 400 mL/24 hours (oliguric phase)
Color: Dirty, brown sediment indicates the presence of RBCs, hemoglobin.
Specific gravity: Less than 1.020 reflects kidney disease, e.g., glomerulonephritis, pyelonephritis.
Protein: High-grade proteinuria (3–4+) strongly indicates glomerular damage when Red Blood Cells and casts are also present
Glomerular filtration rate (GFR): The GFR is a standard means of expressing overall kidney function.

Blood

Serum Creatinine & BUN(BUN/Cr): Elevated,BUN:Cr ratio can sometimes help differentiate causes (>20:1 suggests prerenal).
Complete blood count (CBC): Hemoglobin (Hb) decreased in presence of anemia.
Arterial blood gases (ABGs): Metabolic acidosis (pH less than 7.2) may develop because of decreased renal ability to excrete hydrogen and end products of metabolism.
Chloride, phosphorus, and magnesium, Sodium, Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue release (red cell hemolysis).
Estimated GFR (eGFR): Calculated from creatinine, age, sex, race; tracks function over time (less accurate in rapidly changing AKI).

Imaging

Renal ultrasound: Essential first step. Assesses kidney size (small suggests CKD), checks for hydronephrosis (indicating postrenal obstruction), evaluates renal vasculature (Doppler). Determines kidney size and presence of masses, cysts, obstruction in upper urinary tract.
Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters. ● Renal arteriogram: Assesses renal circulation and identifies extravascularities, masses.
Voiding cystourethrogram: Shows bladder size, reflux into ureters, retention.
Non Nuclear computed tomography (CT) scan: Cross-sectional view of kidney and urinary tract detects presence/extent of disease.
Magnetic resonance imaging (MRI): Provides information about soft tissue damage.
Excretory urography (intravenous urogram or pyelogram): Radiopaque contrast concentrates in urine and facilitates visualization of KUB(Kidney, Ureter, Bladder)

Kidney Biopsy:

Performed when the cause of AKI is unclear after initial workup, especially if intrinsic glomerular disease (GN) or interstitial nephritis (AIN) is suspected.
Involves taking a small sample of kidney tissue via a needle, usually under ultrasound guidance, for microscopic examination. Helps guide specific treatment.

Management of Acute Renal Failure

Aims:

Primary Goal: Identify and treat the underlying cause promptly!

Prerenal: Restore renal perfusion (fluids, blood products, improve cardiac output).
Intrarenal: Stop nephrotoxic agents, treat underlying infection/inflammation (e.g., steroids for AIN/some GN), supportive care for ATN.
Postrenal: Relieve the obstruction (e.g., Foley catheter for bladder outlet obstruction, ureteral stents, nephrostomy tubes).
Restore Normal Chemical Balance: The primary goal is to stabilize electrolytes, acid-base balance, and fluid volume within safe ranges.
Prevent Complications: Prevent or manage complications that can arise during the course of acute renal failure, such as fluid overload, electrolyte disturbances, hypertension, and infections, until renal function recovers.

In-Hospital Management:

1. Admission and Rest: Admit the patient to a monitored setting and ensure adequate rest to minimize energy expenditure. Assist with daily activities to conserve energy.

2. Fluid and Salt Restriction:

Fluid Restriction: Limit fluid intake to 600 ml per day plus the previous day’s fluid loss. This helps prevent fluid overload and edema.
Salt Restriction: Limit salt intake to less than 2 grams per day (about half a teaspoon). This reduces fluid retention and helps control blood pressure.

3. Fluid Balance Monitoring:

Fluid Balance Chart: Accurately monitor fluid intake and output (urine, vomit, diarrhea) using a fluid balance chart to assess fluid balance and adjust fluid intake accordingly.
Overload Prevention: Avoid overloading the patient with fluids by adjusting fluid intake based on the individual’s needs and fluid losses.

4. Edema Assessment:

Edema Monitoring: Regularly assess for edema (swelling) in the extremities, skin turgor, and fontanelles (in infants) to identify fluid overload or dehydration.

5. Symptom Management:

Antiemetics (ondansetron, metoclopramide – dose adjust) for nausea, laxatives for constipation, anticonvulsants (levetiracetam often preferred due to renal clearance profile) if seizures occur. Vitamin supplements may be needed if nutrition poor.

6. Vital Signs Monitoring:

Blood Pressure: Monitor blood pressure twice daily to detect hypertension or hypotension. Antihypertensives if needed, avoiding agents that worsen renal perfusion in certain settings (e.g., ACEi/ARBs if bilateral RAS suspected). Low dose dopamine is NOT recommended for renal protection/vasodilation – proven ineffective.
Weight: Weigh the patient twice daily to assess fluid balance.
Other Vital Observations: Monitor other vital signs such as temperature, heart rate, and respiratory rate.

7. Dialysis:Dialysis (Renal Replacement Therapy – RRT): Used when supportive measures fail to control life-threatening complications. Removes waste products, excess fluid, and corrects electrolyte/acid-base imbalances. Dialysis is considered in severe cases to address:

Fluid Overload: Dialysis can help remove excess fluid, reducing edema, pulmonary edema, and congestive heart failure.
Hyperkalemia (High Potassium Levels): Dialysis removes excess potassium from the blood, preventing potentially life-threatening complications.
Elevated BUN (Blood Urea Nitrogen): Dialysis can help lower elevated BUN levels, a marker of kidney function.
Severe Hypertension: Dialysis can help control severe hypertension that is not responsive to medications.
Metabolic Acidosis: Dialysis can help correct metabolic acidosis, a condition where the body produces too much acid.

Types of Dialysis:

Hemodialysis: This involves filtering the blood through a machine outside the body.
Peritoneal Dialysis: This involves using the patient’s peritoneal membrane (lining of the abdomen) as a filter.

Indications of Dialysis (AEIOU mnemonic):

Acidosis: Severe metabolic acidosis refractory to bicarbonate therapy.
Electrolytes: Severe, refractory hyperkalemia.
Intoxications: Dialyzable drug overdoses or toxins (e.g., methanol, ethylene glycol, lithium, salicylates).
Overload: Fluid overload refractory to diuretics, causing respiratory compromise.
Uremia: Symptomatic uremia (encephalopathy, pericarditis, severe bleeding).

8. Fluid and Electrolyte Replacement/Management:

Fluid Management: Critical. Requires meticulous monitoring of intake (oral, IV) and output (urine, drains, GI losses) plus estimation of insensible losses (~500-1000 mL/day). Aim for euvolemic (normal fluid balance). Fluid restriction is often needed in the oliguric phase. Careful IV fluid selection (isotonic preferred, avoid potassium-containing fluids if hyperkalemic). In diuretic phase, it may need significant fluid replacement to prevent dehydration. Daily weights are essential.
Electrolyte Correction: Monitor and replace/restrict electrolytes (Na+, K+, Ca++, Phos) as needed based on lab values.

9. Nutritional Therapy:

Goal: Provide adequate calories to prevent catabolism (muscle breakdown, which increases BUN), while managing electrolyte and fluid restrictions.
Consultation: Renal dietitian consultation is highly recommended. Enteral or parenteral nutrition may be required if oral intake is inadequate.
Calories: High calorie intake often needed due to hypermetabolic state, especially in critical illness. Primarily carbohydrates and fats.
Protein: Needs are controversial in AKI. Severe restriction may hinder tissue repair. Moderate intake (0.8-1.2 g/kg/day) often recommended, may increase with dialysis. Needs individualized based on catabolic state and dialysis modality. Moderate protein intake, but provide adequate calories to meet energy needs. Protein restriction helps reduce the burden on the kidneys.
Electrolyte Restrictions: Potassium, phosphate, and sodium intake usually need to be limited, especially in the oliguric phase.

Low-potassium foods: Apples, berries, cabbage, carrots, green beans, grapes, rice.
Avoid high-potassium foods: Bananas, oranges, potatoes, tomatoes, spinach, dried fruits, salt substitutes.

Diet Considerations: Consider a balanced diet with adequate calories and vitamins, limiting foods high in potassium, sodium, and phosphorus.

10. Electrolyte and Urine Monitoring:

Electrolytes: Frequently check electrolyte levels (sodium, potassium, calcium, magnesium) to identify and correct imbalances.
Urine Output: Monitor urine output closely to assess kidney function and adjust treatment as needed.

11. Infection Treatment:

Antibiotics if infection is present/suspected. Choose agents carefully and adjust doses based on estimated renal function (eGFR). Prefer antibiotics not primarily cleared by the kidneys if possible (e.g., some macrolides like azithromycin, chloramphenicol, doxycycline) or those easily dose-adjusted.

12. Complications Management:

Hypertension: Administer antihypertensive medications to control blood pressure.
Convulsions: Treat seizures with anticonvulsant medications.
Infections: Promptly treat any infections with appropriate antibiotics.

13. Metabolic Acidosis:

Sodium Bicarbonate: Administer sodium bicarbonate 50-100 mcg to correct metabolic acidosis, which occurs when the body produces too much acid. IV Sodium Bicarbonate may be given for severe acidosis (pH < 7.1-7.2 or HCO3 < 10-12), but use cautiously due to sodium/fluid load. Dialysis corrects acidosis effectively.
Sodium Bicarbonate Mechanism: Sodium bicarbonate helps restore the acid-base balance in the body, reducing the excess acid.

14. Hyperkalemia Management:

IV Dextrose 50%, Insulin, and Calcium: Administer intravenous dextrose 50%, insulin, and calcium replacement to shift potassium back into cells, lowering blood potassium levels.
Diuretic Agents: Diuretic agents can also be used to control fluid volume and aid in potassium excretion.
Antagonize Cardiac Effects: IV Calcium Gluconate or Calcium Chloride (stabilizes cardiac membrane, does not lower K+).
Shift K+ into Cells: IV Insulin with Glucose, Sodium Bicarbonate (if acidotic), Beta-agonists (albuterol nebulized).
Remove K+ from Body: Potassium-binding resins (e.g., Sodium Polystyrene Sulfonate (Kayexalate), Patiromer, Sodium Zirconium Cyclosilicate), Loop Diuretics, Dialysis (most effective).

15. Skin Integrity:

Pressure Area Care: Provide proper care of pressure areas to prevent skin breakdown, particularly in severely ill patients.
Regular Turning: Turn patients regularly to relieve pressure points and promote circulation.

16. Nephrotoxic Drug Suspension:

Stop Nephrotoxic Drugs: Stop any medications that may be toxic to the kidneys (nephrotoxic drugs).

17. Shock Management:

Hemorrhagic Shock: Treat shock with blood transfusions in cases of hemorrhagic shock to replace blood loss.

Nursing Management of AKI:

Assessment:

Frequent vital signs (BP, HR, RR, Temp).
Strict Intake & Output (often hourly). Calculate fluid balance.
Daily weights (same time, scale, clothing).
Assess for fluid overload: Edema, JVD, lung sounds (crackles), shortness of breath, S3 heart sound.
Assess for dehydration (especially diuretic phase): Skin turgor, mucous membranes, orthostatic hypotension.
Monitor lab results: BUN, Cr, electrolytes (esp. K+), ABGs, CBC. Report critical values promptly.
ECG monitoring for signs of hyperkalemia (peaked T waves, wide QRS).
Assess mental status, neurological checks.
Monitor for signs of infection (fever, tachycardia, site redness/drainage).
Assess nutritional status, appetite, GI symptoms.
Skin integrity assessment (risk of breakdown due to edema, immobility).
Assess dialysis access site (catheter) if present.

Nursing Diagnoses:

Fluid Volume Excess (related to decreased GFR/urine output, sodium retention).
Risk for Deficient Fluid Volume (related to excessive loss during diuretic phase).
Risk for Decreased Cardiac Output (related to fluid overload, electrolyte imbalance, acidosis).
Inadequate nutrition (related to anorexia, nausea, dietary restrictions, catabolism).
Risk for Infection (related to uremia, invasive lines/procedures).
Risk for Electrolyte Imbalance (Hyperkalemia, Hypocalcemia, etc.).
Decreased Activity tolerance (related to anemia, uremia, fluid imbalance).
Excessive Anxiety (related to critical illness, uncertain prognosis).
Knowledge Deficit (regarding condition, treatment, diet).

Interventions:

Administer medications as ordered, monitoring for effects and side effects. Adjust doses based on renal function.
Implement fluid restrictions/replacements accurately. Maintain IV therapy.
Monitor patient response to diuretics and dialysis.
Maintain meticulous aseptic technique with all lines and procedures. Catheter care.
Monitor for and prevent complications (hyperkalemia, fluid overload, infection, bleeding, skin breakdown).
Provide nutritional support, assist with meals, monitor intake.
Frequent repositioning, skin care.
Provide patient and family education about AKI, treatments, diet, and follow-up.
Provide emotional support and reassurance.
Collaborate with multidisciplinary team (physicians, dietitians, pharmacists, social workers).

CHRONIC RENAL FAILURE

CKD is defined as abnormalities of kidney structure or function, present for more than 3 months, with implications for health. It involves a progressive, slow, insidious, and irreversible decline in renal excretory and regulatory functions.

Criteria: Either GFR < 60 mL/min/1.73 m² for >3 months, OR markers of kidney damage (e.g., albuminuria [ACR ≥ 30 mg/g], urine sediment abnormalities, electrolyte abnormalities due to tubular disorders, histological abnormalities, structural abnormalities on imaging, history of kidney transplant) present for >3 months.

Chronic Kidney Disease (CKD): The broader term encompassing all stages of chronic kidney damage/reduced function.

Chronic Renal Failure (CRF): Often used to describe later stages of CKD when GFR is significantly reduced and complications are prominent.

End-Stage Renal Disease (ESRD): The final stage (Stage 5 CKD), where kidney function is insufficient to sustain life, requiring renal replacement therapy (dialysis or transplantation). GFR is typically < 15 mL/min/1.73 m². This stage is characterized by uremia, the syndrome of symptoms resulting from the accumulation of toxic waste products.

Causes of Chronic Renal Failure:

Major Causes:

Diabetes Mellitus (Diabetic Nephropathy): Leading cause (~40-50%). High blood glucose damages glomerular capillaries.
Hypertension (Hypertensive Nephrosclerosis): Second leading cause (~25-30%). High blood pressure damages small blood vessels in the kidneys.

Other Causes:

Glomerulonephritis: Chronic inflammation of the glomeruli (e.g., IgA nephropathy, FSGS).
Polycystic Kidney Disease (PKD): Inherited disorder causing multiple cysts in the kidneys.
Chronic Pyelonephritis: Recurrent kidney infections causing scarring.
Chronic Tubulointerstitial Nephritis: Long-term damage to tubules/interstitium (e.g., from drugs like lithium, chronic NSAID use, heavy metals).
Obstructive Uropathy: Long-term blockage (e.g., untreated BPH, congenital anomalies).
Vascular Diseases: Renal artery stenosis, atheroembolic disease.
Autoimmune Disorders: Systemic Lupus Erythematosus (SLE), scleroderma, vasculitis.
Nephrotoxic Agents (Long-term exposure): Certain medications, heavy metals.
Kidney Stones (Nephrolithiasis): Recurrent stones can cause damage/obstruction.
Congenital Abnormalities: Structural kidney problems present from birth.
Risk Factors: Family history of kidney disease, older age, ethnicity (African American, Hispanic, Native American, Asian American have higher risk), obesity, smoking, cardiovascular disease.

Pathophysiology of CKD Progression:

Initial Kidney Damage: Due to underlying etiology (diabetes, HTN, etc.).
Nephron Loss: Gradual destruction of functioning nephrons.
Compensatory Hypertrophy & Hyperfiltration: Remaining nephrons enlarge and increase their individual filtration rate to compensate for the loss. This maintains overall GFR initially.
Intraglomerular Hypertension: Increased pressure and flow within the remaining glomeruli.
Maladaptive Consequences: This hyperfiltration, while initially compensatory, eventually becomes damaging. It leads to further glomerular injury (glomerulosclerosis), proteinuria, and interstitial fibrosis.
Progressive Nephron Loss: A vicious cycle ensues where compensation leads to further damage and loss of more nephrons.
Declining GFR: As nephron mass falls below a critical level, overall GFR begins to decline steadily.
Uremia: When GFR falls significantly (typically <15-20 mL/min), waste products accumulate to toxic levels, and regulatory functions fail, leading to the clinical syndrome of uremia affecting multiple organ systems.

Stages of CKD (Based on GFR and Albuminuria – KDIGO Guidelines): Staging helps guide management.

Stage	GFR (mL/min/1.73 m²)	Description	Clinical Action
1	≥ 90	Kidney damage, normal GFR	Diagnose/treat underlying cause, reduce CV risk
2	60-89	Kidney damage, mild ↓ GFR	Estimate progression, continue risk reduction
3a	45-59	Mild-moderate ↓ GFR	Evaluate & treat complications (anemia, bone disease)
3b	30-44	Moderate-severe ↓ GFR	More aggressive complication management
4	15-29	Severe ↓ GFR	Prepare for Renal Replacement Therapy (RRT)
5	< 15 (or dialysis)	Kidney Failure (ESRD)	RRT (Dialysis or Transplant) required for survival

(Albuminuria is also staged: A1 <30, A2 30-300, A3 >300 mg/g creatinine – higher albuminuria indicates higher risk at any GFR stage)

Clinical Manifestations of CKD (Uremic Syndrome)

Develop gradually as GFR declines, affecting nearly every organ system. Many symptoms are nonspecific initially.

Neurological:

Early: Fatigue, lethargy, impaired concentration, irritability, depression, sleep disturbances.
Late: Peripheral neuropathy (restless legs syndrome, burning feet, paresthesias), asterixis, muscle twitching, encephalopathy (confusion, disorientation, memory loss), seizures, coma.
Cognitive impairment is common.

Cardiovascular (Leading cause of death in CKD):

Hypertension: Very common (due to fluid/sodium retention, RAAS activation).
Heart Failure: Due to volume overload, hypertension, anemia, uremic cardiomyopathy.
Left Ventricular Hypertrophy (LVH).
Arrhythmias: Especially due to hyperkalemia, hypocalcemia, structural changes.
Pericarditis: Inflammation of the pericardial sac due to uremic toxins. Can lead to pericardial effusion and tamponade.
Accelerated Atherosclerosis: Increased risk of MI, stroke, peripheral vascular disease (due to traditional risk factors plus inflammation, oxidative stress, lipid abnormalities, Ca/Phos issues).
Pitting Edema: Due to fluid retention.

Hematologic:

Anemia: Normocytic, normochromic. Primarily due to decreased erythropoietin (EPO) production by failing kidneys. Iron deficiency (absolute or functional) and B12/folate deficiency can contribute. Causes fatigue, weakness, pallor, reduced exercise tolerance.
Bleeding Tendency: Platelet dysfunction (impaired adhesion/aggregation) due to uremic toxins. Leads to easy bruising, prolonged bleeding time.
Impaired Immune Function: Increased susceptibility to infections (WBC dysfunction).

Gastrointestinal:

Anorexia, nausea, vomiting (especially in the morning).
Uremic Fetor: Ammonia-like odor on the breath (breakdown of urea in saliva).
Metallic taste (dysgeusia).
Mouth ulcerations (stomatitis), bleeding gums.
Constipation or diarrhea.
GI bleeding (uremic gastritis/colitis, platelet dysfunction).

Pulmonary:

Pulmonary edema (“uremic lung” on CXR) due to fluid overload. Causes dyspnea, orthopnea, crackles.
Pleuritis/Pleural effusion (similar mechanism to pericarditis).
Kussmaul respirations (deep, rapid breathing) due to severe metabolic acidosis.
Thick, tenacious sputum. Increased risk of pneumonia.

Metabolic / Endocrine:

Metabolic Acidosis: Impaired acid excretion and bicarbonate regeneration.
Electrolyte Imbalances: Hyperkalemia, Hyperphosphatemia, Hypocalcemia (late), Hypermagnesemia (less common unless intake high). Sodium may be high/low/normal.
Carbohydrate Intolerance: Insulin resistance, impaired insulin degradation (may lead to lower insulin needs in diabetics as CKD progresses).
Hyperlipidemia: Altered lipid metabolism (high triglycerides, low HDL).
Secondary Hyperparathyroidism: Complex process: ↓GFR → ↑Phosphate → ↓Calcium (binds phosphate) & ↓Active Vit D → ↑Parathyroid Hormone (PTH) secretion → PTH tries to ↑Calcium and ↓Phosphate by acting on bone and kidney → Leads to Renal Osteodystrophy.

Musculoskeletal:

Renal Osteodystrophy: Bone disease resulting from Ca/Phos/VitD/PTH imbalances. Includes osteitis fibrosa cystica (high turnover bone disease due to high PTH), osteomalacia (low turnover), adynamic bone disease (low turnover). Causes bone pain, increased fracture risk, muscle weakness.

Dermatologic:

Generalized itching (Pruritus): Common and distressing. Cause multifactorial (uremic toxins, dry skin, high Phos/PTH).
Dry skin (xerosis).
Pallor (due to anemia).
Ecchymoses (easy bruising) due to platelet dysfunction.
“Uremic Frost“: Crystallized urea deposits on skin (rare now with earlier dialysis).
Thin, brittle nails; thin, dry hair.

Genitourinary / Reproductive:

Early: Nocturia (loss of concentrating ability).
Late: Oliguria or Anuria.
Sexual dysfunction: Decreased libido, erectile dysfunction (men), menstrual irregularities/infertility (women).

Diagnostic Evaluations for CKD:

Blood Tests: BUN, Creatinine (monitor trends, calculate eGFR), Electrolytes (K, Na, Cl, HCO3, Ca, Phos), Magnesium, Parathyroid Hormone (PTH), Vitamin D levels, CBC (anemia), Iron studies (ferritin, TSAT), Lipid profile, Albumin (nutritional status), HbA1c (if diabetic).
Urine Tests: Urinalysis (protein, blood, glucose, sediment for casts), Urine Albumin-to-Creatinine Ratio (ACR) (quantifies albuminuria – key marker of damage and risk), 24-hour urine collection (for measured CrCl or protein – less common now).
Renal Biopsy: Sometimes performed if the cause of CKD is unclear, especially if a treatable condition like certain glomerulonephritides is suspected. Less common than in AKI.
CBC: Assess for anemia.
Imaging Studies:

Renal Ultrasound: Assess kidney size (typically small and echogenic in CKD, except in PKD or diabetic nephropathy where they can be normal/large initially), rule out obstruction, evaluate for cysts/masses.
CT/MRI: Less routine, used for specific indications (e.g., suspected malignancy, complex anatomy)

Management of CKD

Aims of Management

Focuses on slowing progression, managing complications, and preparing for RRT. Requires a multidisciplinary approach.

1. Slowing Progression:

Blood Pressure Control: Strict control is crucial! Target typically <130/80 mmHg (may vary). ACE inhibitors or ARBs are often first-line, especially in patients with proteinuria/albuminuria, due to renoprotective effects beyond BP lowering.
Glycemic Control: Tight control in diabetics (target HbA1c ~7% or individualized). SGLT2 inhibitors and GLP-1 agonists have shown significant renoprotective benefits in diabetic kidney disease.
Treat Underlying Cause: Address glomerulonephritis, infections, obstruction if possible.
Avoid Nephrotoxins: NSAIDs, contrast dye (if possible), certain antibiotics.
Smoking Cessation.
Weight Management.

2. Managing Complications:

Fluid & Sodium Management: Sodium restriction (usually <2g/day), fluid restriction may be needed in later stages if edema/hypertension present. Loop diuretics (furosemide) often required.
Hyperkalemia: Dietary potassium restriction, review medications (stop K-sparing diuretics, ACEi/ARBs may need dose adjustment/caution), potassium binders (patiromer, sodium zirconium cyclosilicate) for chronic management.
Metabolic Acidosis: Oral alkali therapy (sodium bicarbonate or sodium citrate) if serum bicarbonate falls consistently below 22 mEq/L.
Hyperlipidemia: Statins recommended for cardiovascular risk reduction.
Cardiovascular Disease Prevention: Manage BP, lipids, glucose; aspirin (if indicated); lifestyle modifications.
Mineral and Bone Disorder (CKD-MBD):
Phosphate Control: Dietary phosphate restriction, Phosphate binders taken with meals (Calcium carbonate/acetate initially; non-calcium binders like sevelamer, lanthanum preferred if calcium high or vascular calcification present).
Calcium/Vitamin D: Maintain normal calcium levels. Vitamin D supplementation (often active form like calcitriol or analogues) if deficient and PTH high. Avoid excessive calcium intake.
PTH Control: Use Vitamin D analogues, Calcimimetics (e.g., cinacalcet – increases sensitivity of calcium-sensing receptor on parathyroid gland) to lower PTH if severely elevated despite other measures. Parathyroidectomy in refractory cases.
Anemia:
Rule out/treat iron deficiency (oral or IV iron).
Erythropoiesis-Stimulating Agents (ESAs) like epoetin alfa, darbepoetin alfa to stimulate RBC production. Target hemoglobin typically 10-11.5 g/dL (higher targets associated with risks).

Medications

Antibiotics:

– Class: Antibiotics are medications used to treat bacterial infections.

– Examples: Common antibiotics used for kidney infections include fluoroquinolones (e.g., ciprofloxacin, levofloxacin), cephalosporins (e.g., ceftriaxone, cephalexin), and

trimethoprim/sulfamethoxazole.

– Side Effects: Potential side effects may include gastrointestinal upset, allergic reactions, rash, photosensitivity, and rarely, serious adverse events like tendon rupture (in the case of fluoroquinolones).

– Contraindications: Contraindications may include known allergies to the medication, certain medical conditions, or interactions with other medications. It’s important to discuss your medical history and current medications with your healthcare provider.

Analgesics:

– Class: Analgesics are medications used to relieve pain.

– Examples: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or acetaminophen (paracetamol) may be used for pain relief in kidney infections or diseases.

– Side Effects: Common side effects of NSAIDs include gastrointestinal upset, stomach ulcers, and kidney problems if used excessively or for a prolonged period. Acetaminophen should be used cautiously in patients with underlying liver disease or if taken in excessive amounts.

– Contraindications: Contraindications may include known allergies to the medication, certain medical conditions (e.g., gastric ulcers, liver disease), or interactions with other medications. Discuss your medical history and current medications with your healthcare provider.

Diuretics:

– Class: Diuretics are medications that increase urine output and help remove excess fluid from the body.

– Examples: Diuretics commonly used in kidney diseases include loop diuretics (e.g., furosemide) and thiazide diuretics (e.g., hydrochlorothiazide).

– Side Effects: Common side effects may include electrolyte imbalances, dehydration, dizziness, and increased urination.

– Contraindications: Contraindications may include known allergies to the medication, certain medical conditions (e.g., severe electrolyte imbalances, kidney failure), or interactions with other medications. Your healthcare provider will assess your specific situation.

3. Nutritional Therapy:

Protein: Moderate protein restriction (e.g., 0.6-0.8 g/kg/day) may help slow progression in pre-dialysis stages (controversial, needs careful monitoring to avoid malnutrition). Once on dialysis, protein needs increase (1.0-1.2 g/kg/day for HD, higher for PD) due to losses during treatment.
Calories: Ensure adequate caloric intake (25-35 kcal/kg/day) to prevent catabolism.
Sodium, Potassium, Phosphate: Restrictions individualized based on lab values and stage.
Fluid: Restriction often necessary in later stages/on dialysis.
Vitamins: Water-soluble vitamins (B complex, C) may need supplementation, especially with dialysis losses. Avoid high doses of Vitamin A (fat-soluble, accumulates).
Requires Renal Dietitian: Essential for education and meal planning.

4. Preparation for Renal Replacement Therapy (RRT):

Initiate discussions and education about RRT options (hemodialysis, peritoneal dialysis, transplantation) ideally in Stage 4 CKD.
Timely placement of dialysis access (AV fistula/graft for HD, PD catheter for PD) well before RRT is needed.
Evaluation for kidney transplantation (living or deceased donor).

5. Renal Replacement Therapy (RRT): Initiated in ESRD (Stage 5).

Hemodialysis (HD): Blood filtered outside the body via a machine. Usually done 3 times/week for 3-5 hours per session, typically in a dialysis center (can be done at home). Requires vascular access (AV fistula preferred, AV graft, or central venous catheter).
Peritoneal Dialysis (PD): Uses the patient’s own peritoneal membrane as the filter. Dialysis fluid (dialysate) is instilled into the abdominal cavity via a surgically placed catheter, dwells for a period, and then drained. Can be done manually several times a day (CAPD) or overnight using a machine (APD). Done at home by the patient.
Kidney Transplantation: Surgical placement of a healthy kidney from a living or deceased donor. Offers the best quality of life and survival but requires lifelong immunosuppression to prevent rejection. Not all patients are suitable candidates.

Nursing Management of CKD:

Focuses on long-term care, education, adherence, monitoring, and supporting the patient through disease progression and RRT.

Assessment:

Monitor vital signs, daily weights, intake/output.
Assess for signs/symptoms of uremia and complications (fluid overload, electrolyte imbalance, anemia, bone disease, neurological changes, cardiovascular issues, infection).
Review lab results (GFR trends, electrolytes, CBC, Ca/Phos/PTH, albumin).
Assess nutritional status, adherence to dietary/fluid restrictions.
Medication reconciliation – ensure appropriate drugs and doses for renal function.
Assess psychosocial status, coping mechanisms, knowledge level.
If on dialysis: Assess access site (fistula/graft: bruit/thrill; PD catheter: exit site infection signs), monitor treatment tolerance.
If post-transplant: Monitor for rejection, infection, medication side effects.

Nursing Diagnoses: Similar to AKI but reflect chronicity.

Fluid Volume Excess.
Inadequate Nutrition intake.
Risk for Infection.
Decreased Activity tolerance.
Risk for Injury (related to bone disease, neuropathy, falls).
Disrupted Body Image (related to access, fluid shifts, skin changes).
Ineffective Coping / Anxiety / Depression.
Knowledge Deficit (complex regimen, RRT options).
Risk for Decreased Cardiac Output.
Risk for Impaired Skin Integrity (related to edema, pruritus, access devices).
Sexual Dysfunction.

Interventions:

Patient Education: Crucial for self-management. Teach about CKD, stages, importance of adherence to diet (Na, K, Phos, fluid, protein limits), medications (purpose, side effects, timing – e.g., phosphate binders with meals), BP/glucose monitoring, recognizing complications, RRT options.
Medication Management: Administer meds, monitor effects, reinforce importance of adherence.
Dietary/Fluid Management: Reinforce dietitian’s recommendations, help patient find acceptable food choices, monitor intake.
Monitoring & Surveillance: Track labs, weights, vitals. Assess for complications.
Symptom Management: Strategies for pruritus (moisturizers, cool baths, antihistamines if ordered), nausea (antiemetics, small frequent meals), fatigue (pacing activities, anemia management).
Access Care: Meticulous care of HD or PD access sites to prevent infection/complications. Teach patient self-care.
Psychosocial Support: Encourage expression of feelings, identify coping strategies, refer to support groups or counseling if needed. Address body image concerns.
Coordination of Care: Collaborate with nephrologist, dietitian, social worker, transplant team, primary care physician.
Promote Activity: Encourage activity as tolerated to maintain strength and well-being.
Prevent Complications: Infection control, fall prevention, skin care

General Nursing Interventions of Renal / kidney diseases

1. Monitor vital signs: Regularly assess and record the patient’s blood pressure, heart rate, respiratory rate, and temperature to detect any changes or abnormalities.

2. Assess fluid status: Monitor the patient’s fluid intake and output, including urine output, to evaluate fluid balance and detect any signs of fluid overload or dehydration.

3. Administer medications as prescribed: Ensure timely administration of prescribed medications, including diuretics, antihypertensives, phosphate binders, erythropoiesis-stimulating agents, and other medications specific to the patient’s condition.

4. Monitor laboratory values: Regularly monitor renal function tests (e.g., serum creatinine, blood urea nitrogen) and electrolyte levels (e.g., sodium, potassium) to assess kidney function and guide treatment decisions.

5. Provide dietary guidance: Collaborate with a registered dietitian to develop an appropriate meal plan, considering the patient’s specific renal disease, stage, and dietary restrictions (e.g., limiting sodium, potassium, phosphorus intake).

6. Assess and manage pain: Evaluate the patient’s pain level, provide appropriate pain management strategies, and monitor the effectiveness of pain relief interventions.

7. Educate about self-care: Teach patients about proper self-care techniques, including medication management, monitoring fluid and dietary restrictions, and recognizing signs of complications or worsening symptoms.

8. Monitor for signs of infection: Be vigilant for signs and symptoms of urinary tract infections (UTIs) or other infections and promptly initiate appropriate treatment if necessary.

9. Assist with dialysis or renal replacement therapy: If the patient requires dialysis or other renal replacement therapies, provide support, educate about the procedure, and monitor for any complications or adverse reactions.

10. Promote physical activity: Encourage patients to engage in regular physical activity within their capabilities to promote overall health, manage weight, and improve cardiovascular fitness.

11. Provide emotional support: Recognize the emotional impact of renal disease on patients and their families, and offer emotional support, counseling, or referrals to support groups or mental health professionals as needed.

12. Monitor and manage fluid balance: Assess for signs of fluid overload or dehydration and collaborate with the healthcare team to adjust fluid management strategies accordingly.

13. Prevent complications: Implement preventive measures to minimize the risk of complications such as pressure ulcers, deep vein thrombosis (DVT), and infections.

14. Monitor and manage electrolyte imbalances: Regularly assess electrolyte levels and implement appropriate interventions to correct imbalances, such as administering electrolyte supplements or adjusting the patient’s diet.

15. Provide wound care: If the patient has surgical wounds or access sites (e.g., arteriovenous fistula, catheter), ensure proper wound care techniques and monitor for any signs of infection or complications.

16. Promote optimal nutrition: Collaborate with the dietitian to optimize the patient’s nutritional status, including ensuring adequate protein intake and addressing any specific dietary needs or restrictions.

17. Educate about medication management: Provide education on the importance of taking medications as prescribed, potential side effects, and the need for regular follow-up appointments.

18. Monitor and manage anemia: Assess and monitor the patient’s hemoglobin and hematocrit levels, collaborate with the healthcare team to manage anemia using appropriate interventions such as iron supplementation or erythropoiesis-stimulating agents.

19. Collaborate with the interdisciplinary team: Work closely with other healthcare professionals, such as nephrologists, social workers, and pharmacists, to ensure comprehensive and coordinated care for the patient.

20. Provide patient and family education: Educate patients and their families about their condition, treatment options, lifestyle modifications, and the importance of adherence to the treatment plan

NB. General guidelines & may vary depending on the specific needs of the patient and the stage and severity of their renal or kidney disease.

Renal Failure Read More »

Kidney Stones / Renal Calculi

Kidney Stones/Renal Calculi

Kidney Stones are small, hard deposits of mineral and acid salts on the inner surfaces of the kidneys.

They can also be defined as crystallized minerals around pus, blood or damaged tissues.

Stones are classified by their location in the urinary system and their composition of crystals, they can also be called;

Renal Lithiasis
Renal Calculi
Nephrolithiasis (Kidney Stone Disease)
Urinary stones (urilithiasis)

Most stones consist of calcium salts (calcium oxalate) or magnesium-ammonium phosphate.
Other renal stones are uric acid stones, struvite and cystine stones

Pathophysiology of Kidney Stones

Urinary stones are formed by aggregation/precipitation of mineral crystals deposited in urine.
Most originate in the collecting ducts or renal papillae and pass to the renal pelvis where they may increase in size. Some become too large and fail to pass through the ureters and obstruct the out flow of urine causing kidney damage. Those passed to the bladder are either excreted or increase in size and obstruct the urethra. Some renal stones originate from the bladder
The frequency of different types of renal stones varies between countries due to diet, environmental factors, congenital factors, chronic urinary infection, urine stasis and excessive secretion of stone forming substances.

Causes of Kidney stones

Metabolic diseases: abnormalities that result in increased urine levels of calcium, oxaluric acid or citric acid such as hyperparathyroidism, renal tubular acidosis, medication like diuretics, vitamin C and D abuse and antacids. Other medications include acetazolamide (Diamox) or indinavir (Crixivan)
Diet
Large intake of protein increase uric acid excretion, excessive amounts of tea or fruit juices, elevate urinary oxalate level, large intake of calcium and oxalate and reduced intake of fluid increase concentration of urine
Climate
Warm climates cause increase fluid loss. Low urine volume and increase solute concentration in urine led to stone formation.
Congenital and inherited diseases
Family history of stones formation, cystinuria, gout or renal acidosis, familial hypercalciuria (FHH) and primary oxaluria
Slow urine ﬂow allows accumulation of crystals—damaging the lining of the urinary tract and decreasing the number of inhibitor substances that would prevent crystal accumulation.

Clinical Manifestations

Manifestations depend on the presence of obstruction, infection, and edema. Symptoms range from mild to excruciating pain and discomfort.

Stones in Renal Pelvis

Intense, deep ache in costovertebral region
Hematuria and pyuria
Pain that radiates anteriorly and downward toward bladder in female and toward testes in male
Acute pain, nausea, vomiting, costovertebral area tenderness (renal colic)
Abdominal discomfort, diarrhea

Ureteral Colic (Stones Lodged in Ureter)

Acute, excruciating, colicky, wavelike pain, radiating down the thigh to the genitalia
Frequent desire to void, but little urine passed; usually contains blood because of the abrasive action of the stone (known as ureteral colic)
Uriteric stones led to colicky abdominal pain (flank pain) radiating to the iliac fossa, testis and labia on the same side. There may also be pallor sweating, vomiting , frequency of micturition, dysuria and hematuria

Stones Lodged in Bladder

Symptoms of irritation associated with urinary tract infection and hematuria
Urinary retention, if stone obstructs bladder neck
Possible urosepsis if infection is present with stone
Bladder stones lead to increased frequency of micturition, dysuria, hematuria, severe intraurethral or perineal pain if trigonitis occurs and distended bladder if outflow obstruction
of urine occurs

Diagnosis of Renal Stones

Renal or ureteric stones are suspected on history of colicky abdominal pain with hematuria
The following investigations confirms the diagnosis and should be done to every suspected patient

Xrays of the kidneys, ureters, and bladder or by ultrasonography, to detect size and site of the stones.
IV urography, or retrograde pyelography show hydronephrosis and stone impaction.
CT-Scan to confirm the non radio opaque stones (uric acid stones)
Chemical tests ie urinalysis, serum calcium and serum uric acid levels to determine stone composition.
Blood chemistries and a 24hour urine test for measurement of calcium, uric acid, creatinine, sodium, and urine pH.
CBC: Hb/HCT: Abnormal if patient is severely dehydrated or polycythemia is present (encourages precipitation of solids), or patient is anemic (hemorrhage, kidney dysfunction/failure).
Cystourethroscopy: Direct visualization of bladder and ureter may reveal stone and/or obstructive effects.

Management of Kidney Stones

Acute attack

Aims of management.

Alleviate pain.
Maintain adequate renal functioning.
Prevent complications.
Provide information about disease process/prognosis and treatment needs.

Medical management also aims at to eradicate the stone, determine the stone type, prevent nephron destruction, control infection, and relieve any obstruction that may be present.

Patients with renal stones may be acutely ill suffering from excruciating/piercing pain arising in loin radiating to the groin which can last for 5 – 6 hours due to small calculi being moved along the ureters by peristalsis so bed rest and worth to the site of pain is needed for relief. Read this Research on how rest is important in passing out kidney stones.
Narcotics are use to relieve renal colic’s such as morphine.
Stones less than 5mm are non obstructive and may be passed through the urinary tract to be excreted in urine. Alpha-blockers like tamsulosin can be used to aid passage of renal stones.
Increased fluid intake to assist in stone passage, unless patient is vomiting; patients with renal stones should drink eight to ten glasses of water daily or have IV fluids prescribed to keep the urine dilute.
Take and record observation such as temperature, pulse, respiration, blood pressure and observe for signs of infection such dark colored urine, cloudy urine with abnormal odour e.t.c.
Prochlorperazine is given to treat nausea and vomiting
Do investigation to rule infections and treat the accordingly.
Larger stones more than 1cm can be crushed by extracorporeal shock-waves lithotripsy(ESWL). and removed through urine
Chemo lysis (stone dissolution) which is an alternative for those who are poor risks for other therapies, or have easily dissolved stones (struvite).
Impacted large stone are managed by endoscopic surgery or open surgery (nephrolithotomy or uretero-lithotomy). Surgical removal is performed in only 1% to 2% of patients.

Continuous care/prevention further kidney stone development

Give moderate proteins and restrict sodium in diet
Take 3-4 litres of fluids a day
Diet containing plenty calcium prevents oxalate stones like mils, cheese, ice-cream, yoghurt , all beans, dried fruits and fish with fine bones (sardines, kippers, herring, salmon)
Avoid food rich in oxalate such peanuts, spinach, rhubarb, cabbage, tomatoes, chocolate, cocoa, tea etc
Thiazide diuretics calcium stone in a patient with hypercalciuria
Allopurinol prevent urate stones in hyperuricemia
Avoid vitamin D supplements as they increase calcium absorption and excretion.
Calcium lactate can be given to precipitate oxalate in the GIT or give cholestyramine to bind oxalate and prevent GIT absorption for calcium oxalate stones.
In cystine stones give alpha-penicillamine and tiopronin to prevent crystallization. In all types stones give potassium citrate to maintain alkalinity of urine

SPECIFIC NURSING MANAGEMENT

Pain Management: Assess the patient’s pain level and administer pain relief medications as prescribed. Monitor the effectiveness of pain management and document pain levels.
Fluid Intake: Encourage the patient to drink plenty of fluids to help flush out the stones and prevent dehydration. Adequate hydration can reduce the risk of stone formation.
Monitoring Vital Signs: Regularly check the patient’s vital signs, including blood pressure, heart rate, and temperature, to identify signs of infection or complications.
Strain Urine: Provide a urine strainer or sieve to the patient and instruct them to strain their urine to catch any stone fragments for analysis. Document the results.
Assessment for Hematuria: Monitor for the presence of blood in the urine (hematuria). Document the color and amount of blood.
Education: Educate the patient about their condition, the importance of following treatment plans, and lifestyle modifications to prevent recurrence.
Nutritional Counseling: Provide guidance on dietary changes that can help reduce the risk of stone formation. This may include recommendations to limit certain foods high in oxalates, salt, and animal proteins.
Ambulation: Encourage the patient to ambulate and stay active, which can facilitate the passage of kidney stones and reduce complications.
Medication Administration: Administer prescribed medications such as alpha-blockers to relax the ureter, helping stones pass more easily, or medications to control pain and manage infections.
Assessment for Signs of Infection: Monitor for signs of urinary tract infections, such as fever, chills, or cloudy and foul-smelling urine. Report any changes to the healthcare provider.
Prevention Measures: Discuss preventive measures with the patient, including increased fluid intake, dietary changes, and lifestyle modifications to reduce the risk of stone recurrence.
Emotional Support: Recognize that kidney stones can be painful and distressing. Offer emotional support to the patient and address any anxiety or concerns they may have about the condition or its treatment.

Diagnosis

Nursing Diagnoses

Acute pain related to inflammation, obstruction, and abrasion of the urinary tract
Deficient knowledge regarding prevention of recurrence of renal stones

Nursing Care Plan

Assessment	Nursing Diagnosis	Expected Outcomes/Goals	Interventions	Rationale	Evaluation
Acute Pain	Acute pain related to tissue trauma evidenced by reports of colicky pain, restlessness, moaning, facial mask of pain.	- Report pain is relieved with spasms controlled. - Appear relaxed, able to sleep/rest appropriately.	- Determine and note location, duration, intensity (0–10 scale), and radiation of pain -. Document nonverbal signs such as elevated BP and pulse, restlessness, moaning.	- Aids to evaluate site of obstruction and progress of calculi movement. - Justify and clarify cause of pain and the need of notifying caregivers of changes in pain occurrence and characteristics.	The patient did not complain or report any pain episode. - Patient was relaxed and was able to get sleep appropriately.
Failure to pass urine.	Impaired Urinary Elimination related to inflammation or obstruction of the bladder by calculi, renal or ureteral irritation as evidenced by urgency and frequency of urination(oliguria) and haematuria.	- Pass urine in normal amounts and usual pattern. - Experience no signs of obstruction.	- Record input and output and characteristics of urine. - Encourage the patient to walk if possible. - Promote sufficient intake of fluids. - Investigate reports of bladder fullness; palpate for suprapubic distension. Note decreased urine output, presence of periorbital and dependent edema.	- Provides information about kidney function and presence of complications (infection and hemorrhage) - To facilitate spontaneous passage. - Calculi may cause nerve excitability, which causes sensations of urgent need to pass urine. - Increased hydration flushes bacteria, blood, and debris and may facilitate stone passage. - Urinary retention may develop, causing tissue distension (bladder, kidney), and potentiates risk of infection, renal failure.	- Patient was able to pass urine in sufficient amounts following a usual pattern. - Obstruction was relieved.
Dehydration	Risk for Deficient Fluid Volume may be related to nausea and vomiting	- Maintain adequate fluid balance as evidenced by vital signs and weight within patient’s normal range, palpable	- Monitor and document fluid input and output and daily weight. - Promote fluid intake to 3–4 L a day within cardiac tolerance.	- Comparing actual and anticipated output may aid in evaluating presence and degree of renal stasis or impairment. - Maintains fluid balance for homeostasis and “washing” action that may flush the stone(s) out.	its potential Dx, so it hasn't happened

Complications of Kidney Stones.

Obstruction: One of the most common complications is the obstruction of the urinary tract. Small stones can obstruct the flow of urine, causing severe pain and discomfort. Larger stones may block the ureter or urethra completely, leading to excruciating pain and potential damage to the kidneys.
Infections: When urine flow is obstructed, bacteria can grow in the stagnant urine, leading to urinary tract infections (UTIs). UTIs can cause symptoms like fever, chills, and pain during urination.
Kidney Damage: Prolonged obstruction of urine flow can damage the kidneys. Kidney function may deteriorate, leading to kidney failure if the condition is not treated promptly.
Hematuria: Kidney stones can cause bleeding in the urinary tract, leading to blood in the urine (hematuria). This can be painful and may indicate injury to the urinary tract.
Recurrence: Some individuals are more prone to developing kidney stones, and they may experience recurrent episodes over time.
Severe Pain: The passage of kidney stones through the urinary tract can cause severe pain, commonly referred to as renal colic. This pain can be debilitating and may require medical intervention for relief.
Complications during Pregnancy: Kidney stones can pose a risk to pregnant women. If a stone becomes trapped in the urinary tract during pregnancy, it can lead to complications and require specialized care.
Formation of New Stones: Having kidney stones once increases the risk of developing more in the future. Patients with a history of kidney stones should take measures to prevent their recurrence.

Kidney Stones / Renal Calculi Read More »

Cystitis

CYSTITIS

Cystitis is a lower lower urinary infection involving inflammation of the urinary bladder.

Acute bacterial cystitis is common in women as the short urethra predisposes them to infection of the bladder.

Causes of Cystitis

Cystitis also arises when there is an obstruction to urine flow, disease inside the urinary bladder duct such as stones and tumor.
Bladder incompetence. The inability to empty the bladder completely could lead to infection.
Bladder tumors. Urine flow is obstructed by the tumor, causing urinary stasis.
Prostrate enlargement, paraplegic patients with loss of bladder control suffer from cystitis due to prolonged and repeated catheterization.
Other diseases like gonorrhea, tuberculosis may cause cystitis.
Ascending infections. More lower UTIs result from ascending infection by a single, gram-negative, enteric bacterium such as Escherichia coli, Klebsiella, Proteus, Enterobacter, Pseudomonas, and Serratia.
Decreased natural host defenses. Immunosuppression and a weak immune system could predispose the patient to infection
> Klebsiella aerogenosa
> Proteus mirabilis
> E-coli and E. faecalis contributes to 80% of all cases
> Streptococcus faecalis
> Chlamydia
> Neisseria gonorrhoea
> Mycobacterium

Common Clinical Presentation of cystitis

Dysuria (painful urination)
Nocturia. The patient experiences awakening at night to urinate.
Urethral discharge. The presence of discharge is also possible, especially in males.
Frequency and urgency of urination
Pyuria (making urine cloudy)/WBCs
Fever
Haematuria
Tenderness on the suprapubic region (lower abdominal pain burning in nature)
Foul smelling urine
Nausea and vomiting
Fatigue and anorexia
Bacteriuria

Investigation of cystitis

Urinalysis of the midstream urine to rule out proteins, pus, infecting organism (microscopy confirms the organisms)
Blood for urea and creatine
Cystoscopy/ intravenous pyelography
A CT scan may detect pyelonephritis or abscesses.
Ultrasonography is extremely sensitive for detecting an obstruction, abscesses, tumors, and cysts.
Cellular studies. A patient with cystitis usually has microscopic hematuria and pyuria.
Leukocyte esterase test. A multiple-test dipstick often includes testing for WBCs.

Management of Cystitis

Appropriate antibiotics after urine culture and sensitivity for 7 days to 10 days
Ciprofloxacin 250mg to 500mg bd
Nitrofurantoin 100mg 8 hourly for 5 days or
Cotrimoxazole 960 to 480mg 12 hourly
Ampicillin or gentamycin
Relieve pain with analgesics
Give plenty of fluids to flush the bladder and reduce irritation of the bladder
Examine urine periodically
Avoid bladder irritants like coffee, alcohol, citrus juice, chocolate, beverages and highly spiced foods
Health educate the patient on preventive interventions of UTIs and treatment adherence
Adequate rest promotes healing
Use condom/abstain from sex during treatment
Improve perianal hygiene and avoid sharing bathing basins and towels

Prevention or Patient advice

Maintain hydration. Suggest drinking plenty of fluids, i.e. water(8litres a day)
Urinate promptly. Tell the patient to urinate promptly whenever the urge arises.
Maintain hygiene. Wiping from front to back after urinating and after bowel movement helps prevent bacteria in the anal region from spreading to the vagina and urethra.
Sexual hygiene. After intercourse, the bladder should be emptied as soon as possible.
Avoid irritation. Use of deodorant sprays and other feminine products, such as douches and powders, should be avoided because that may irritate the urethra.
Compliance. Strict compliance with the medication regimen ensures non resistance of bacteria from the drug

Nursing Care Management

Nursing Diagnosis	Planning	Goal/Outcome	Intervention	Evaluation
Acute pain related to infection within the urinary tract.	Relieve pain and discomfort within 2 hours	Relief of pain and discomfort.	- Suggest a warm sit bath for relief of perineal discomfort -Administer prescribed analgesics	Patient was relieved of pain and was comfortable within 2 hours.
Deficient knowledge related factors predisposing the patient to infection and recurrence, characterized by patient asking a lot of questions.	Increase knowledge of the patient about preventive measures and the treatment modalities.	Increased knowledge of preventive measures and treatment modalities.	-Education about nature & purpose of the treatment and emphasize the importance of drug compliance.	Patient understood uses of drug compliance and preventive measures.

URETHRITIS

Urethritis is the inflammation of the urethra.

It co-exists with cystitis, which makes it harder to diagnose.

Causes of Urethritis

Trichomonas and monilial infection are causes of urethritis in women.
In men urethritis is commonly caused by Chlamydia and gonorrhea
Other bacterial infection like in cystitis
Viral organisms like herpes.
Non infective urethritis is due to chemicals like deodorants spray and drugs.

Signs and symptoms of Urethritis

(a) Urethral discharge is cardinal in the diagnosis
(b) Pain in urination and urethral itching.
(c) Other signs as in cystitis

Investigations

Urine culture to isolate organisms
As in cystitis

Management of Urethritis

Give doxycycline 100mg 12 hourly to treat chlamydia infection
Trichomonas is treated with metronidazole 200 – 400mg 8 hourly for 7 days
Moniliasis infection is treated with nystatin or fluconazole
Treat pain with analgesics
Ciprofloxacin 250mg to 500mg
Nitrofurantoin 100mg 8 hourly for 5 days or
Cotrimoxazole 960 to 480mg 12 hourly
Hot sit bath gives relief to women
Improve perianal hygiene
Stop using deodorants and chemicals causing urethritis
Stop intercourse during treatment

Cystitis Read More »

Urinary Tract Infections

Urinary Tract Infections (UTIs)

Urinary tract infections (UTIs) are bacterial infections that can occur in any part of the urinary system, including the kidneys, bladder, ureters, and urethra.

The most common cause of UTIs is the colonization of bacteria from the gastrointestinal tract, with Escherichia coli (E. coli) being the most frequently implicated pathogen. Other pathogens that can cause UTIs include Klebsiella, Proteus, Enterococcus, and Staphylococcus species.

At its core, a UTI is defined as an infection in any part of the urinary system. This system, responsible for filtering waste and producing urine, comprises several key organs:

Kidneys: These bean-shaped organs are the primary filters of the blood, removing waste products and excess fluid to form urine.
Ureters: These are thin tubes that transport urine from each kidney to the bladder.
Bladder: A muscular sac that stores urine until it’s ready to be expelled from the body.
Urethra: The tube that carries urine from the bladder out of the body during urination.

While UTIs can occur in any part of this system, the majority of infections are localized in the lower urinary tract, specifically involving the bladder (cystitis) and the urethra (urethritis). Infections affecting the kidneys are termed pyelonephritis and represent a more serious form of UTI.

Prevalence of Urinary Tract Infections

UTIs are significantly more prevalent in women than in men, particularly in the younger to middle-aged adult population (20-50 years). In this age bracket, women are approximately 50 times more likely to develop a UTI compared to men. This striking difference is primarily attributed to anatomical differences, specifically the shorter urethra in females, which allows bacteria easier access to the bladder.

However, the landscape of UTI prevalence shifts with age. While UTI incidence increases in both sexes beyond 50 years of age, the female-to-male ratio decreases. This is largely due to the increasing occurrence of prostate enlargement (benign prostatic hyperplasia – BPH) and instrumentation (medical procedures involving insertion of instruments into the urethra) in men as they age. BPH can lead to urinary retention, and instrumentation can introduce bacteria, both increasing UTI risk in men.

Specific Types of UTIs based on Location and Demographics:

Women (20-50 years): The most common types of UTIs in this group are cystitis (bladder infection) and pyelonephritis (kidney infection). These are often considered “uncomplicated” UTIs in otherwise healthy, non-pregnant women without structural urinary tract abnormalities.
Men (20-50 years): In men of the same age, UTIs are less frequent but often present as urethritis (urethral infection) or prostatitis (prostate infection). UTIs in men are generally considered more complex and require thorough evaluation.
Older Adults (>50 years): The incidence of UTIs increases in both sexes. In women, cystitis and pyelonephritis remain common. In men, alongside urethritis and prostatitis, UTIs may become associated with BPH and require careful management.

Risk Factors for Urinary Tract Infections

UTIs develop when bacteria, usually from the bowel, enter the urinary tract and multiply. Several factors can compromise the body’s natural defenses and increase the likelihood of bacterial colonization and infection. These risk factors can be broadly categorized:

1. Iatrogenic/Drugs (Medical Procedure or Medication Related):

Indwelling Catheters: These tubes, inserted into the urethra to drain urine, provide a direct pathway for bacteria to enter the bladder. Catheter-associated UTIs (CAUTIs) are a significant concern, especially in hospitalized patients.
Antibiotic Use: While antibiotics treat infections, their overuse can disrupt the normal, protective bacterial flora in the vagina and bowel. This disruption can allow pathogenic bacteria (like E. coli, a common UTI culprit) to flourish and colonize the urinary tract more easily.
Spermicides: These chemicals, used for contraception, can irritate the vaginal area and alter the normal vaginal flora, increasing susceptibility to UTI.

2. Behavioral Factors:

Voiding Dysfunction: Conditions or habits that prevent complete bladder emptying, such as infrequent urination or bladder muscle problems, can lead to post-void residual urine. This stagnant urine provides a breeding ground for bacteria.
Frequent or Recent Sexual Intercourse: Sexual activity can introduce bacteria into the urethra, particularly in women. “Honeymoon cystitis” is a term sometimes used to describe UTIs related to increased sexual activity.

3. Anatomic/Physiologic Factors:

Vesicoureteral Reflux (VUR): This condition involves the abnormal backflow of urine from the bladder into the ureters and sometimes up to the kidneys. VUR causes urinary retention, giving bacteria more time to grow. The retrograde flow also allows bacteria to ascend higher into the urinary tract, potentially reaching the kidneys.
Female Sex: As mentioned, the shorter urethra in females makes it easier for bacteria from the perineal area to reach the bladder.
Pregnancy: Hormonal changes during pregnancy, particularly increased progesterone, cause smooth muscle relaxation in the bladder and ureters. Additionally, the growing uterus can compress the ureters. Both these factors can lead to urinary retention, increasing the risk of UTI.

4. Genetic Predisposition:

Familial Tendency: There’s evidence suggesting a genetic component to UTI susceptibility, as UTI occurrence can cluster in families.
Susceptible Uroepithelial Cells: The cells lining the urinary tract (uroepithelial cells) play a role in defense against infection. Some individuals may have uroepithelial cells that are more susceptible to bacterial adhesion and invasion.
Vaginal Mucus Properties: The properties of vaginal mucus, including its composition and viscosity, can influence the ability of E. coli to bind and colonize.

Pathophysiology of Urinary Tract Infections

Colonization: The process often begins with bacteria, typically from the bowel flora, colonizing the periurethral area (the skin around the urethral opening). These bacteria then ascend through the urethra, moving upwards towards the bladder. E. coli is the most frequent culprit in uncomplicated UTIs due to its ability to adhere to uroepithelial cells.
Uroepithelium Penetration: Certain bacterial features, like fimbriae (pili), act as adhesion molecules. Fimbriae allow bacteria to attach to and penetrate the bladder’s epithelial cells. After penetration, bacteria can replicate within the bladder lining and may form biofilms, communities of bacteria encased in a protective matrix, making them harder to eradicate.
Ascension: If the infection is not contained at the bladder level, bacteria can ascend further up the urinary tract, moving through the ureters towards the kidneys. Factors like VUR can facilitate this ascension. Bacterial toxins may also inhibit peristalsis (the rhythmic contractions of the ureters that help move urine downwards), reducing urine flow and aiding bacterial ascent.
Pyelonephritis: When bacteria reach the kidneys and infect the renal parenchyma (the functional tissue of the kidney), it triggers an inflammatory response known as pyelonephritis. This kidney infection can be severe. While usually caused by ascending bacteria, pyelonephritis can also result from hematogenous spread – bacteria traveling from another infection site in the body through the bloodstream to the kidneys (though this is less common in typical UTIs).
Acute Kidney Injury: If the inflammatory cascade in the kidney continues unchecked, it can lead to tubular obstruction (blockage of the kidney tubules) and tissue damage, resulting in interstitial edema (swelling in the kidney tissue). This process can progress to interstitial nephritis, ultimately causing acute kidney injury (AKI).

Etiology of Urinary Tract Infections

Common Bacterial Culprits

The vast majority of UTIs are caused by bacteria. Identifying the common culprits is crucial for effective treatment.

Most Frequent Cause (Enteric Gram-Negative Aerobic Bacteria):

Escherichia coli (E. coli): This bacterium is the dominant cause, responsible for 75-95% of cystitis and pyelonephritis cases in uncomplicated UTIs. E. coli is a normal inhabitant of the bowel but can become pathogenic when it enters the urinary tract.
Klebsiella species: Another common gram-negative bacterium found in the gut.
Proteus mirabilis: Known for its ability to produce urease, an enzyme that can raise urine pH, potentially leading to the formation of struvite kidney stones.
Pseudomonas aeruginosa: While less common in uncomplicated UTIs, Pseudomonas is more frequently seen in catheter-associated infections and complicated UTIs, often exhibiting antibiotic resistance.

Less Frequent Cause (Gram-Positive Bacteria):

Staphylococcus saprophyticus: This gram-positive coccus is a significant cause of UTIs, particularly in young, sexually active women (5-10% of bacterial UTIs in this group).
Enterococcus faecalis (Group D streptococci): Enterococci are becoming increasingly important UTI pathogens, especially in hospitalized patients and those with complicated UTIs.
Streptococcus agalactiae (Group B streptococci): While primarily known for neonatal infections, Group B strep can also cause UTIs in adults, including pregnant women.

Clinical Presentation: Signs and Symptoms of Urinary Tract Infections

The symptoms of a UTI vary depending on the location of the infection within the urinary tract.

1. Kidney Infection (Acute Pyelonephritis): Symptoms are typically more systemic and severe:

Upper back and side (flank) pain: Pain is often localized to the area of the affected kidney.
High fever: Elevated body temperature is a common sign of systemic infection.
Shaking chills: Rigors, or uncontrollable shaking, can accompany fever.
Nausea and Vomiting: Gastrointestinal symptoms are frequent.
General malaise and fatigue: Feeling unwell and weak.

2. Bladder Infection (Cystitis): Symptoms are more localized to the lower urinary tract:

Pelvic pressure: A feeling of discomfort or fullness in the lower pelvis.
Lower abdomen discomfort: Pain or cramping in the lower abdomen.
Frequent, painful urination (dysuria): A hallmark symptom of cystitis, characterized by urgency and pain during urination.
Blood in urine (hematuria): Urine may appear pink, red, or tea-colored due to blood.
Suprapubic tenderness: Pain when pressing on the area just above the pubic bone.

3. Urethral Infection (Urethritis): Primarily characterized by:

Burning with urination: Pain and a burning sensation during urination.
Discharge: Urethral discharge may be present, especially if the urethritis is sexually transmitted.

Classification of UTIs: Uncomplicated vs. Complicated

UTIs are broadly classified into uncomplicated and complicated, which has significant implications for management.

Uncomplicated UTI:

Typically occurs in premenopausal adult women.
No underlying structural or functional abnormalities of the urinary tract.
Not pregnant.
No significant comorbidities (other health conditions) that would increase the risk of treatment failure or serious outcomes.
Usually involves cystitis or pyelonephritis in this specific demographic.

Complicated UTI:

A UTI is considered complicated if any of the following are present:

Patient Demographics:

Child: UTIs in children require different considerations.
Pregnancy: Pregnancy significantly alters UTI management.
Male Sex: UTIs in men are generally considered complicated due to the potential for underlying prostate involvement.
Any Age Beyond Premenopausal Women: UTIs in older individuals or those outside the typical demographic for uncomplicated UTI often have underlying factors.

Underlying Conditions:

Structural or Functional Urinary Tract Abnormality: Conditions like kidney stones, obstructions, neurogenic bladder, or VUR can complicate UTIs.
Comorbidities Increasing Infection Risk: Conditions such as poorly controlled diabetes, chronic kidney disease, immunocompromised states (e.g., HIV, organ transplant recipients), or sickle cell disease increase the complexity of UTI management.
Recent Instrumentation or Surgery of the Urinary Tract: Procedures like cystoscopy or urological surgery can introduce bacteria and complicate UTI.

Diagnosis of Urinary Tract Infection

Urine Collection: Proper urine collection is essential to avoid contamination and ensure accurate results.

Clean-catch, Midstream Specimen: This is the preferred method for routine UTI diagnosis. Patients are instructed to clean the genital area, start urinating, and then collect the mid-portion of the urine stream into a sterile container, avoiding the initial and final portions. This helps minimize contamination from the urethra and surrounding skin.
Specimen Obtained by Catheterization: In certain situations, such as in patients unable to void voluntarily or those with indwelling catheters, urine may be collected directly through catheterization. This method is more invasive but can be necessary for specific patient populations.
Urethral Swab for STD Testing (if suspected): If a sexually transmitted infection (STD) is suspected as a cause of urethritis (e.g., in men with urethral discharge), a urethral swab for STD testing should be obtained prior to voiding to avoid washing away the organisms.

Urine Testing:

Dipstick Tests: These are rapid, point-of-care tests that can provide preliminary information about urine.

Nitrate Positive: A positive nitrate test is highly specific for UTI. Many bacteria, especially gram-negative bacteria like E. coli, can convert nitrates (normally present in urine) to nitrites. However, the nitrate test is not very sensitive; a negative result doesn’t rule out UTI.
Leukocyte Esterase Test: This test detects leukocyte esterase, an enzyme released by white blood cells (leukocytes). A positive leukocyte esterase test is very specific for the presence of increased white blood cells (> 10 WBCs/µL) in the urine, indicating inflammation, and is fairly sensitive for UTI.

Microscopic Examination: Microscopic analysis of urine sediment provides more detailed information.

Pyuria: The presence of white blood cells in urine is called pyuria. Most truly infected patients have pyuria with > 10 WBCs/µL. Pyuria is a key indicator of UTI, but it can also be present in other inflammatory conditions of the urinary tract.
Bacteria: The presence of bacteria in urine (bacteriuria) is another important finding. However, bacteria can be present due to contamination during sampling, even without a true UTI. If bacteria are seen without pyuria, contamination is more likely.
Microscopic Hematuria: Small amounts of blood in the urine (microscopic hematuria) are common in UTIs, occurring in up to 50% of patients. Gross hematuria (visible blood in urine) is less common.
WBC Casts: These are cylindrical structures formed in the kidney tubules and composed of white blood cells. WBC casts suggest kidney involvement and can be seen in pyelonephritis, glomerulonephritis, and noninfective tubulointerstitial nephritis.

Urine Culture: A urine culture is the gold standard for confirming UTI and identifying the specific bacteria causing the infection. It involves growing bacteria from the urine sample in a lab to determine the type of bacteria and its quantity. Culture is particularly recommended in:

Complicated UTIs: To guide antibiotic selection in complex cases.
Pregnant women: Due to the significance of UTI in pregnancy.
Postmenopausal women: Often have more complex UTIs.
Men: UTIs in men are generally considered complicated.
Prepubertal children: Require careful evaluation and culture.
Patients with urinary tract abnormalities or recent instrumentation: To identify unusual pathogens or resistant organisms.
Patients with immunosuppression or significant comorbidities: Increased risk of treatment failure or resistant infections.
Patients with symptoms suggesting pyelonephritis or sepsis: To guide appropriate antibiotic therapy for severe infections.
Patients with recurrent UTIs (≥ 3/year): To identify potential underlying causes and guide preventive strategies.

Urinary Tract Imaging: Imaging studies are not routinely needed for simple cystitis but are indicated in certain situations to assess for structural abnormalities or complications.

Ultrasound, CT Scan, IVU (Intravenous Urogram): These are common imaging choices for evaluating the urinary tract.

Voiding Cystourethrography (VCUG), Retrograde Urethrography, Cystoscopy: These more specialized procedures may be warranted in specific cases to visualize the urethra, bladder, and assess for reflux or obstructions.

Indications for Imaging in Adults:

≥ 2 Episodes of Pyelonephritis: Recurrent kidney infections may suggest underlying anatomical issues.
Complicated Infections: Imaging helps assess for structural factors contributing to complicated UTIs.
Suspected Nephrolithiasis (Kidney Stones): Stones can predispose to UTI and cause obstruction.
Painless Gross Hematuria or New Renal Insufficiency: These findings may indicate more serious underlying conditions.
Fever Persists for ≥ 72 hours Despite Antibiotics: Suggests possible complications or antibiotic resistance.
Children with UTI: Often require imaging to rule out congenital urinary tract abnormalities, especially VUR.

Types of Urinary Tract Imaging and Their Uses:

KUB Ultrasound (First-line, Non-invasive)

MCUG (Contrast Radiographic Imaging)

Nuclear Scans (DMSA & MAG3 Radioisotope)

Uses

Assess: Fluid collections, Bladder volume, Kidney size/shape/location, Urinary tract obstructions/dilatations

Uses

Confirm: Posterior urethral valves, Obstructive Uropathies, Gold standard for VUR diagnosis

Uses

Confirm: Suspicion of renal damage, DMSA: Gold standard for renal scar detection, MAG3: Faster/less radiation, Renal excretion enables micturition study

Indications

– Concurrent bacteremia,
– Atypical UTI organisms (Staph aureus, Pseudomonas), |
– UTI <3 years old,
– Non/inadequate response to 48h of IV antibiotics,
– Abdominal mass,
– Abnormal voiding,
– Recurrent UTI,
– First febrile UTI and no prompt follow up assured,
– Renal impairment,
– Significant electrolyte derangement,
– No antenatal renal tract imaging in 2nd/3rd trimester

Indications

– Abnormal renal ultrasound (Hydronephrosis, Thick bladder wall, Renal scarring),
– Abnormal voiding post-febrile UTI,
– Post-second febrile UTI,
– Suspicion of VUR,
– Posterior urethral valves

Indications

– Clinical suspicion of renal injury,
– Reduced renal function, – Suspicion of VUR,
– Suspicion of obstructive uropathy on ultrasound in older toilet-trained children

Limitations

Does not assess function, Operator dependent, Cannot diagnose VUR

Limitations

Radiation exposure ~1 mSv, Invasive, Unpleasant post-infancy, May need sedation, Requires prophylactic antibiotics

Limitations

Dynamic renal excretion study requires toilet training, False positives if <3 months post-UTI (not for acute phase), May need sedation, Cannot determine old vs. new scarring

KUB-Ultrasound of Kidney, ureters and bladder also known as ultrasound KUB
MCUG-Micturating Cystogram

Differential Diagnosis of Urinary Tract Infection

Acute Urethral Syndrome (in women): This syndrome involves dysuria, frequency, and pyuria, mimicking cystitis. However, unlike cystitis, routine urine cultures in acute urethral syndrome are often negative. Causative organisms may be different or the inflammation may be non-infectious.
Urethritis (non-bacterial): Urethritis can be caused by sexually transmitted infections like Chlamydia trachomatis and Ureaplasma urealyticum. These organisms are not typically detected on routine urine cultures for bacterial UTI. STD testing is essential in sexually active individuals with urethritis symptoms.
Noninfectious Causes: Several non-infectious conditions can mimic UTI symptoms:

Anatomic abnormalities: Urethral stenosis (narrowing).
Physiologic abnormalities: Pelvic floor muscle dysfunction.
Hormonal imbalances: Atrophic urethritis (common in postmenopausal women due to estrogen deficiency).
Localized trauma: Injury to the urethra or bladder.
Gastrointestinal (GI) system symptoms and inflammation: Conditions like appendicitis or inflammatory bowel disease can sometimes present with urinary symptoms.

Management of Urinary Tract Infections

UTI management depends on the type of UTI (uncomplicated vs. complicated), location of infection, patient demographics, and presence of underlying conditions.

Urethritis Management: For sexually active patients with urethritis symptoms, presumptive treatment for STDs is often initiated while awaiting test results. This is because STDs are common causes of urethritis in this population.

Typical Regimen: Combination therapy targeting common STDs:

Ceftriaxone 250 mg IM (intramuscular) single dose (to cover gonorrhea).
Plus either Azithromycin 1 g PO (oral) once or Doxycycline 100 mg PO bid (twice daily) for 7 days (to cover chlamydia).

Cystitis Management (Uncomplicated Cystitis in Non-pregnant Women):

First-line treatment: Short-course antibiotic therapy is usually effective.

Nitrofurantoin 100 mg PO bid for 3 days: A commonly used first-line agent. Contraindicated if creatinine clearance is < 60 mL/min (impaired kidney function).
Trimethoprim/sulfamethoxazole (TMP/SMX) 160/800 mg PO bid for 3 days: Another effective option, but resistance rates may be a concern in some areas.

Acute Pyelonephritis Management: Pyelonephritis necessitates antibiotic treatment.

Outpatient vs. Inpatient Treatment: Outpatient oral antibiotic therapy is possible if all of the following criteria are met:

Patient is expected to be adherent to treatment.
Patient is immunocompetent.
Patient has no nausea or vomiting, or evidence of volume depletion or septicemia (signs of severe infection).
Patient has no factors suggesting complicated UTI.

Outpatient Oral Antibiotic Options:

Ciprofloxacin 500 mg PO bid for 7 days: A quinolone antibiotic effective for pyelonephritis.
Trimethoprim/sulfamethoxazole (TMP/SMX) 160/800 mg PO bid for 14 days: A longer course is often used for pyelonephritis compared to cystitis.

Alternative Management : These are not primary treatments for active infections but may provide symptomatic relief or supportive care.

Cranberry Concentrates (for adults): May help prevent recurrent UTIs, but evidence for treating active infections is limited.
Increase Fluid Intake: Drinking plenty of water helps dilute urine and flush out bacteria.
Ural (urine alkaliniser): May help reduce urinary discomfort by making urine less acidic.

Management in Specific Patient Groups:

Children:

Infants <3 months with fever (T≥38°C): Refer urgently to paediatrics. These infants require prompt evaluation and likely intravenous antibiotics due to the risk of serious infection.
Infants 3 months to 3 years with fever (T≥38°C): Assess for UTI. Consider urine MCS (microscopy, culture, sensitivity) and broad-spectrum antibiotics (IV or PO) +/- IV fluids if UTI is suspected. Paediatric referral may be needed.
Febrile children >3 years: Urinalysis is the first step. Dipstick results (nitrites and leukocyte esterase) can guide management. Urine culture is often needed. Treatment strategies range from oral antibiotics to IV antibiotics depending on clinical severity and dipstick findings.
Antibiotics for Children: Common antibiotics and therapeutic doses for children include:

Trimethoprim (TMP) ‘Alprim’: 4 mg/kg BD (twice daily), Max 150 mg BD.
Trimethoprim-sulfamethoxazole (TMP-SMX) ‘Bactrim’: 4 + 20 mg/kg BD, Max: 160 + 180 mg BD.
Cephalexin ‘Keflex’: 12.5mg/kg QID (four times daily), Max: 500 mg QID.
Amoxicillin and Clavulanic acid ‘Augmentin’: 22.5 + 3.2 mg/kg BD, Max: 875 + 125 mg BD.
Nitrofurantoin ‘Macrodantin’: Not generally recommended for therapeutic UTI treatment in children.

Adults:

Non-pregnant Women:

Empirical treatment: Consider for healthy women <65 years with severe or ≥ 3 UTI symptoms.
Dipstick tests: Guide treatment decisions for healthy women <65 years with mild or ≤2 UTI symptoms.
Treat symptomatic LUTI (lower UTI) with a 3-day course of trimethoprim or nitrofurantoin. Exercise caution with nitrofurantoin in the elderly due to potential toxicity.
Obtain urine culture if treatment fails or to guide antibiotic change.

Pregnant Women:

Screen for asymptomatic bacteriuria: Standard quantitative urine culture at the first antenatal visit. Confirm with a second culture.
Do not use dipstick testing to screen for UTI in pregnancy.
Treat asymptomatic bacteriuria in pregnant women with antibiotics.
Treat symptomatic UTI in pregnant women with antibiotics.
Obtain urine culture before starting empiric antibiotics.
7-day course of treatment (amoxicillin, cephalexin, augmentin) is usually sufficient.
Urine culture for test of cure 7 days after completing antibiotic treatment.

Men:

UTIs in men are generally considered complicated.
Consider conditions like prostatitis, chlamydial infection, and epididymitis in the differential diagnosis.
Urine culture is always recommended in men with UTI symptoms.
Quinolones (ciprofloxacin) are preferred antibiotics due to their ability to penetrate prostatic fluid. Nitrofurantoin and cephalosporins are less effective for prostate infections.
Treat bacterial UTI empirically with a quinolone in men with symptoms suggestive of prostatitis.
4-week course of antibiotics is appropriate for prostatitis.
Refer men for urological investigation if they have upper UTI symptoms, fail to respond to antibiotics, or have recurrent UTIs.

Patients on Catheter:

Do not rely on classical UTI symptoms for diagnosis in catheterized patients. Symptoms may be subtle.
Signs suggestive of catheter-associated UTI (CAUTI): New onset or worsening fever, rigors, altered mental status, malaise, lethargy, flank pain, costovertebral angle tenderness, acute hematuria.
Do not use dipstick testing to diagnose UTI in catheterized patients.
Do not treat asymptomatic bacteriuria in catheterized patients.
Do not routinely prescribe antibiotic prophylaxis to prevent symptomatic UTI in patients with catheters.

Prevention of UrinaryTract Infections

Lifestyle measures can help reduce the risk of UTIs, especially recurrent infections.
Drink plenty of liquids, especially water: Helps flush out bacteria.
Drink cranberry juice: May prevent bacterial adhesion (evidence is mixed).
Wipe from front to back after using the toilet: Prevents fecal bacteria from reaching the urethra (for women).
Empty your bladder soon after intercourse: Helps flush out bacteria that may have entered the urethra.
Avoid potentially irritating feminine products: Douches, powders, and sprays can disrupt vaginal flora.
Change your birth control method: Consider alternatives to spermicides or diaphragms if recurrent UTIs are related.
Prophylaxis for Recurrent UTIs (in women experiencing ≥ 3 UTIs/year):
Behavioral measures are first-line. If unsuccessful, antibiotic prophylaxis may be considered.
Continuous Prophylaxis: Low-dose antibiotics taken daily or several times per week. Typically starts with a 6-month trial, may be extended if UTIs recur.
– TMP/SMX 40/200 mg PO once/day or 3 times/week.
– Nitrofurantoin 50 or 100 mg PO once/day.
– Cephalexin 125 to 250 mg PO once/day.
Postcoital Prophylaxis: Single-dose antibiotic taken after sexual intercourse, if UTIs are temporally related to sexual activity.
Postmenopausal Women: Antibiotic prophylaxis similar to premenopausal women. Topical estrogen therapy may be beneficial for women with atrophic vaginitis or urethritis to reduce recurrent UTIs.

Summary of Key Management Points:

Refer infants <3 months with UTI.
Treat children >3 months with UTI using Amoxicillin/Augmentin, send culture and consider ultrasound.
Treat non-pregnant women with 3 days of Nitrofurantoin for uncomplicated cystitis.
Treat asymptomatic bacteriuria in pregnant women.
Consider STI and prostatitis in men with UTI symptoms.
Do not give prophylaxis for adult with catheter and do not treat asymptomatic bacteriuria in catheterized patients.

Complications of Urinary Tract Infections

While most UTIs are treatable, complications can arise, especially if infections are untreated or complicated.

Recurrent Infections: Frequent UTIs, defined as two or more in six months or four or more within a year, can be a significant problem, particularly in women.
Permanent Kidney Damage: Untreated or severe kidney infections (pyelonephritis) can lead to scarring and permanent kidney damage. Chronic kidney infection can also contribute to long-term renal dysfunction.
Increased Risk in Pregnant Women: UTIs in pregnant women, even asymptomatic bacteriuria, are linked to an increased risk of delivering low birth weight or premature infants.
Urethral Narrowing (Stricture) in Men: Recurrent urethritis, especially if caused by sexually transmitted infections like gonococcal urethritis, can lead to urethral strictures, causing difficulty with urination.
Sepsis: This is a potentially life-threatening complication where the infection spreads into the bloodstream and triggers a systemic inflammatory response. Sepsis is more likely if the UTI ascends to the kidneys.

NURSING DIAGNOSIS

Actual Nursing Diagnosis

Impaired Urinary Elimination related to urinary tract infection as evidenced by dysuria, frequency, and lower abdominal discomfort.

Related Factors: Urinary tract infection, inflammation of the bladder and urethra, bacterial irritation of the urinary tract mucosa.

Evidenced By:

Dysuria (painful urination)
Urinary frequency
Urinary urgency
Lower abdominal discomfort
Report of burning sensation during urination
Nocturia

Acute Pain related to urinary tract infection and bladder spasms as evidenced by reports of pelvic pressure, flank pain, and pain rating scale.

Related Factors: Inflammatory process in the urinary tract, bladder spasms secondary to infection, distention of bladder, renal inflammation (in pyelonephritis).

Evidenced By:

Report of pelvic pressure
Report of lower abdominal discomfort
Report of flank pain (if pyelonephritis)
Pain rating using a pain scale (e.g., 5/10)
Guarding behavior of abdomen or flank
Restlessness or irritability

Deficient Knowledge related to prevention and management of urinary tract infections as evidenced by expressed desire for information and questions regarding UTI recurrence.

Related Factors: Lack of prior exposure to information, misinformation, cognitive limitations, information misinterpretation.

Evidenced By:

Verbalization of lack of understanding about UTI causes, prevention, or management.
Questions about how to prevent future UTIs.
Expressed desire for information about UTI.
Inaccurate follow-through of instructions or procedures related to UTI prevention (if observed).

Fatigue related to physiological effects of infection as evidenced by verbal reports of exhaustion and increased need for rest.

Related Factors: Physiological demands of infection (inflammatory response, immune system activation), pain, disrupted sleep patterns due to nocturia and discomfort.

Evidenced By:

Verbal report of feeling tired or exhausted.
Increased need for rest.
Lethargy or malaise (general feeling of discomfort, illness, or unease).
Verbalization of feeling weak or lacking energy.

Potential Nursing Diagnoses

Risk for Deficient Fluid Volume related to increased urinary frequency and potential fever.

Risk Factors: Increased urinary frequency, fever (if present), inadequate fluid intake, vomiting (if pyelonephritis).

Risk for Electrolyte Imbalance related to potential vomiting and altered renal function (especially in pyelonephritis).

Risk Factors: Vomiting (if pyelonephritis), potential renal involvement in infection, dehydration, pre-existing renal conditions (if applicable).

Risk for Impaired Comfort related to medication side effects (e.g., gastrointestinal upset from antibiotics).

Risk Factors: Antibiotic therapy, potential for gastrointestinal side effects of antibiotics (nausea, diarrhea), individual sensitivity to medications.

Urinary Tract Infections Read More »

Anatomy and Physiology of the Renal System

ANATOMY AND PHYSIOLOGY OF THE RENAL SYSTEM

The urinary system is the main excretory system eliminating waste products from blood through urine. Its anatomy consists of two kidneys, each joined to the bladder by the tube called ureter, which conveys urine from the kidneys to the bladder for storage. Following bladder contraction, urine is expelled through the urethra.

Organs of the Urinary System

2 Kidneys: These bean-shaped organs are the primary functional units of the urinary system. They are responsible for:

Filtering blood to remove waste products, excess water, and electrolytes.
Secreting urine, the fluid waste product.
Regulation of blood pressure and red blood cell production.

2 Ureters: These muscular tubes transport urine from the kidneys to the urinary bladder. Peristaltic contractions of the ureter walls help move urine along.

Urinary Bladder: This hollow, muscular organ serves as a reservoir for urine. It expands to store urine and contracts to expel it during urination.

Urethra: This tube conveys urine from the urinary bladder to the outside of the body. It differs in length and function between males and females. In males, it also serves as a passageway for semen.

The urinary system plays a vital role in maintaining homeostasis by:

Regulating fluid volume: The kidneys adjust the amount of water reabsorbed into the bloodstream, thereby controlling blood volume and blood pressure.
Controlling electrolyte balance: The kidneys regulate the levels of various electrolytes, such as sodium, potassium, and calcium, in the blood.
Maintaining acid-base balance: The kidneys help regulate blood pH by excreting acids and bases as needed.

The kidneys produce urine that contains:

Metabolic waste products: These include nitrogenous compounds like urea (from protein metabolism) and uric acid (from nucleic acid metabolism).
Excess ions: such as sodium, potassium, and chloride.
Various toxins and drugs: The kidneys filter out many foreign substances from the blood.

Urine is stored in the bladder until a sufficient volume accumulates, triggering the urge to urinate. Excretion of urine occurs through a coordinated process called micturition (urination or voiding). This involves:

Relaxation of the internal urethral sphincter (involuntary control).
Contraction of the detrusor muscle (the bladder’s muscular wall).
Relaxation of the external urethral sphincter (voluntary control).

Main Functions of the Kidneys (Expanded)

Formation of Urine: This involves three main processes:

Glomerular filtration: Water and small solutes are filtered from the blood into the Bowman’s capsule.
Tubular reabsorption: Essential substances (e.g., glucose, amino acids, water, electrolytes) are reabsorbed from the filtrate back into the blood.
Tubular secretion: Waste products and excess ions are secreted from the blood into the filtrate.

Maintaining Water, Electrolyte, and Acid-Base Balance: The kidneys constantly adjust the composition of urine to maintain the proper balance of these factors in the body.
Excretion of Waste Products: The kidneys eliminate metabolic waste products, toxins, and drugs from the body.
Production and Secretion of Erythropoietin: This hormone stimulates the bone marrow to produce red blood cells in response to low oxygen levels in the blood.
Production and Secretion of Renin: This enzyme plays a crucial role in the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and electrolyte balance.

COMMON TERMS IN URINARY SYSTEM

Proteinuria : Daily excretion of proteins in the urine is more than 150mg. It signifies that the kidney is damaged/ perforated.
Haematuria :Means passing urine containing blood and is due to bleeding into the urinary tract.
Crystalluria : Presence of crystals like oxalates, phosphates in the urine detected by microscopic examination of urine
Glycosuria : Means presence of sugar (glucose) in urine either due to diabetes mellitus or due to renal glycosuria
Azotemia : Increase in the serum concentration of urea and creatinine above their normal values. This occurs when glomerular filtration pressure (GFR) of the kidneys falls due to renal failure. “uremia”.
Oliguria : Diminished urine volume output of urine i.e. 100 mL to 400 mL per day.
Anuria – Complete absence of urine formation i.e zero to 100 mL per day
Dysuria – Difficulty or pain in passing urine
Polyuria – Urine volume above 3 litres per day
Retention of urine – occurs due to obstruction of urine outflow from the bladder, this is relieved by catheterization

The Kidneys

There are two kidneys which lie behind the peritoneum on either side of the vertebral column. In adults, they measure approximately 12 to 14 cm.

The urine is formed in the kidney by the nephrons.

Each kidney has approximately one million nephrons.

The right kidney sits slightly lower than the left kidney. This difference in position is mainly attributed to the presence of the liver, which occupies substantial space on the right side of the abdominal cavity and pushes the right kidney inferiorly.

Kidneys are bean-shaped organs with approximate dimensions of 11 cm in length, 6 cm in width, and 3 cm in thickness. Each kidney weighs around 150 grams. They are embedded within a protective layer of fat, which helps to cushion and hold them in place.

The kidneys and the surrounding renal fat are enclosed by a sheath of fibrous connective tissue called the renal fascia (Gerota’s fascia). This fascia provides further support and helps anchor the kidneys to the posterior abdominal wall.

Organ Relationships

The kidneys are closely associated with several other organs in the abdominal cavity. These relationships are important for understanding potential clinical implications:

Right Kidney:

Superiorly: The right adrenal gland (also known as the suprarenal gland) sits atop the kidney.
Anteriorly: The right lobe of the liver, the duodenum (the first part of the small intestine), and the hepatic flexure of the colon are located in front of the right kidney.
Posteriorly: The diaphragm and the muscles of the posterior abdominal wall (such as the quadratus lumborum and psoas major) lie behind the right kidney.

Left Kidney:

Superiorly: The left adrenal gland is positioned above the left kidney.
Anteriorly: The spleen, stomach, pancreas, jejunum (another part of the small intestine), and the splenic flexure of the colon are located in front of the left kidney.
Posteriorly: Similar to the right kidney, the diaphragm and the muscles of the posterior abdominal wall are behind the left kidney.

Internal Anatomy

The internal structure of the kidney is complex and highly organized, reflecting its critical role in urine formation. Key features include:

Renal Cortex: This is the outer, reddish-brown layer of tissue directly beneath the fibrous capsule. It contains the renal corpuscles (glomeruli and Bowman’s capsules) and the convoluted tubules, which are essential for filtration and reabsorption.
Renal Medulla: This is the inner layer, composed of pale, cone-shaped striations called renal pyramids.
Renal Pyramids: These are triangular structures within the medulla. Their base faces the cortex, and their apex (the renal papilla) projects into a minor calyx. The pyramids consist mainly of collecting ducts and loops of Henle, which concentrate urine.
Renal Columns (Columns of Bertin): These are extensions of the renal cortex that extend inward between the renal pyramids. They provide a pathway for blood vessels and nerves to reach the cortex.
Renal Papilla: This is the narrow, tip of each renal pyramid. It is where the collecting ducts empty urine into the minor calyces.
Calyces (Minor and Major): These are cup-shaped structures that collect urine from the renal papillae. Several minor calyces merge to form a major calyx.
Renal Pelvis: This is a funnel-shaped structure formed by the merging of two or three major calyces. It collects urine and narrows as it exits the kidney as the ureter. The walls of the calyces and renal pelvis are lined with transitional epithelium, which is well-suited to withstand the changes in volume and composition of urine. The walls also contain smooth muscle, which contracts to propel urine.
Hilum: This is the concave medial border of the kidney where the renal artery, renal vein, lymphatic vessels, nerves, and ureter enter and exit the kidney.

Gross Structure and Urine Flow

Urine formation begins in the nephrons (the functional units of the kidney) located in the cortex and medulla. After the urine is formed, it follows a specific pathway:

From the collecting ducts within the renal pyramids.
Through the renal papilla at the apex of the pyramid.
Into a minor calyx.
Several minor calyces merge into a major calyx.
Two or three major calyces combine to form the renal pelvis.
The renal pelvis narrows and becomes the ureter as it leaves the kidney.

Peristalsis, the intrinsic contraction of smooth muscle in the walls of the calyces, renal pelvis, and ureters, propels urine towards the bladder.

Functions of the Kidney

The kidneys perform numerous vital functions to maintain overall health:

1. Filtration of Blood Plasma and Elimination of Wastes:

The kidneys filter blood plasma to remove metabolic waste products such as urea, creatinine, uric acid, and toxins.
This filtration process occurs in the glomeruli, where high pressure forces fluid and small solutes out of the blood and into Bowman’s capsule.

2. Regulation of Blood Volume and Blood Pressure:

The kidneys regulate blood volume by adjusting the amount of water reabsorbed into the bloodstream or excreted in urine.
They also play a key role in the renin-angiotensin-aldosterone system (RAAS), which helps to control blood pressure by regulating sodium and water balance.

3. Regulation of Fluid Osmolarity:

The kidneys maintain the osmolarity (solute concentration) of body fluids by controlling the amount of water and electrolytes excreted in urine.
This is crucial for preventing cells from swelling or shrinking due to changes in fluid balance.

4. Secretion of Renin:

Renin is an enzyme secreted by the kidneys that initiates the RAAS pathway.
This pathway leads to the production of angiotensin II, which causes vasoconstriction (narrowing of blood vessels) and stimulates the release of aldosterone, a hormone that increases sodium and water reabsorption.

5. Secretion of Erythropoietin (EPO):

EPO is a hormone produced by the kidneys in response to low oxygen levels in the blood (hypoxia).
EPO stimulates the bone marrow to produce more red blood cells, increasing the oxygen-carrying capacity of the blood.

6. Regulation of PCO2 and Acid-Base Balance:

The kidneys help regulate blood pH by excreting acids (such as hydrogen ions) and bases (such as bicarbonate ions) in urine.
They also work with the respiratory system to maintain the proper balance of carbon dioxide (PCO2) in the blood.

7. Synthesis of Calcitriol (Vitamin D):

The kidneys convert a precursor molecule into calcitriol, the active form of vitamin D.
Calcitriol promotes calcium absorption from the intestines, which is essential for bone health and other bodily functions.

8. Detoxification of Free Radicals and Drugs:

The kidneys help to eliminate free radicals (unstable molecules that can damage cells) and detoxify certain drugs.
They contain enzymes that can neutralize free radicals and convert drugs into forms that can be excreted in urine.

9. Gluconeogenesis:

During prolonged fasting or starvation, the kidneys can synthesize glucose from amino acids and other non-carbohydrate sources through a process called gluconeogenesis.
This helps to maintain blood glucose levels when carbohydrate intake is limited.

The Nephron: Functional Unit of the Kidney

Each kidney contains approximately 1 to 2 million functional units called nephrons, alongside a significantly smaller number of collecting ducts.

The nephron is responsible for the actual filtration, reabsorption, and secretion processes that lead to urine formation.

These are the functional (urine) forming units of the kidneys

The collecting ducts serve to transport urine through the renal pyramids to the calyces, contributing to the characteristic striped appearance of the pyramids.

Supporting the collecting ducts is connective tissue, housing blood vessels, nerves, and lymphatic vessels, which are essential for the function and maintenance of these structures.

Nephron Structure

Essentially, a nephron consists of a tubule closed at one end and connected to a collecting duct at the other. The closed end forms the glomerular capsule (Bowman’s capsule), a cup-shaped structure that almost entirely encloses the glomerulus, a network of tiny arterial capillaries.

The glomerulus is a cluster of capillary loops resembling a coiled tuft.

Extending from the glomerular capsule, the nephron tubule measures approximately 3 cm in length and comprises three main parts:

Proximal Convoluted Tubule (PCT): This is the initial, coiled portion of the nephron tubule extending from the Bowman’s capsule, primarily responsible for reabsorbing water, ions, and nutrients from the filtrate.
Medullary Loop (Loop of Henle): This hairpin-shaped structure dips into the renal medulla and plays a critical role in concentrating urine. It consists of a descending limb (permeable to water) and an ascending limb (actively transports sodium chloride).
Distal Convoluted Tubule (DCT): This is the final, coiled portion of the nephron tubule, responsible for further reabsorption of ions and water under hormonal control. It empties into a collecting duct.

The collecting ducts ultimately merge to form larger ducts, which then empty into the minor calyces.

Renal Blood Supply

The kidneys receive approximately 20% of the cardiac output, reflecting their critical role in filtering the blood.

Upon entering the kidney at the hilum, the renal artery branches into smaller arteries and arterioles.

In the cortex, an afferent arteriole enters each glomerular capsule and then subdivides into a cluster of tiny arterial capillaries, forming the glomerulus.

Nestled between these capillary loops are connective tissue phagocytic mesangial cells, which form a crucial part of the monocyte-macrophage defense system, responsible for clearing debris and regulating glomerular filtration.

The blood vessel exiting the glomerulus is the efferent arteriole.

The afferent arteriole possesses a larger diameter than the efferent arteriole, which elevates the pressure inside the glomerulus and facilitates filtration across the glomerular capillary walls.

The efferent arteriole then branches into a second peritubular capillary network, which surrounds the remainder of the tubule, facilitating exchange between the fluid in the tubule and the bloodstream, maintaining a local supply of oxygen and nutrients, and removing waste products.

Venous blood drains from this capillary bed into the renal vein, which ultimately empties into the inferior vena cava.

The walls of the glomerulus and the glomerular capsule are composed of a single layer of flattened epithelial cells. The glomerular walls exhibit greater permeability compared to those of other capillaries. The remainder of the nephron and the collecting duct are formed by a single layer of simple squamous epithelium.

Both sympathetic and parasympathetic nerves supply the renal blood vessels.

This dual innervation allows for precise control of renal blood vessel diameter and renal blood flow, independent of autoregulation mechanisms.

Processes Involved in urine formation

Urine formation involves three primary processes:

Filtration:
Selective Reabsorption:
Secretion:

FILTRATION

Filtration occurs across the semipermeable membrane formed by the glomerulus and Bowman’s capsule. Water and small solutes readily pass through this membrane, while larger molecules like blood cells and plasma proteins are retained in the capillaries.

The resulting filtrate closely resembles plasma in composition but lacks the larger proteins and blood cells.

The driving force for filtration is the pressure gradient between the blood pressure in the glomerulus and the pressure within Bowman’s capsule.

The glomerular capillary hydrostatic pressure (HPA) is maintained at approximately 7.3 kPa (55 mmHg) due to the efferent arteriole being narrower than the afferent arteriole.

This pressure is opposed by:

The osmotic pressure of the blood (OPB), mainly due to plasma proteins, which is approximately 4 kPa (30 mmHg).
The filtrate hydrostatic pressure (HPF) within Bowman’s capsule, which is approximately 2 kPa (15 mmHg).

Net Filtration Pressure (NFP)

The net filtration pressure (NFP) determines the overall rate of filtration. It is calculated as follows:

NFP = HPA – (OPB + HPF)

Using the values above:

NFP = 55 mmHg – (30 mmHg + 15 mmHg) = 10 mmHg

This positive net filtration pressure of 10 mmHg forces fluid and solutes out of the glomerular capillaries and into Bowman’s capsule.

Glomerular Filtration Rate (GFR)

The glomerular filtration rate (GFR) is the volume of filtrate formed by both kidneys per minute.

In a healthy adult, the GFR is approximately 125 mL/min, which equates to 180 liters of filtrate produced by the two kidneys each day.

Remarkably, most of this filtrate is reabsorbed later in the kidney tubules, with less than 1% (1-1.5 liters) being excreted as urine.

The differences in volume and concentration between the initial filtrate and the final urine are due to the processes of selective reabsorption and tubular secretion.

Autoregulation of GFR

Renal blood flow and, consequently, glomerular filtration are protected by a mechanism called autoregulation. Autoregulation maintains a relatively constant renal blood flow across a wide range of systolic blood pressures (approximately 80-200 mmHg).

Autoregulation operates independently of nervous control, meaning it continues to function even if the nerve supply to the renal blood vessels is disrupted.

This mechanism is inherent to the renal blood vessels and may be stimulated by changes in blood pressure within the renal arteries or by fluctuations in the levels of certain metabolites, such as prostaglandins.

However, in cases of severe shock, when systolic blood pressure falls below 80 mmHg, autoregulation fails, and renal blood flow and hydrostatic pressure decrease, impairing filtration within the glomeruli.

SELECTIVE REABSORPTION

Selective reabsorption is the process by which substances are transported from the filtrate back into the blood.

Most reabsorption occurs in the proximal convoluted tubule (PCT), whose walls are lined with microvilli to increase the surface area for absorption. Many substances are reabsorbed here, including water, electrolytes (sodium, potassium, chloride, etc.), and organic nutrients (glucose, amino acids).

Reabsorption can occur through passive or active transport mechanisms:

Passive Transport: This involves the movement of substances across the tubular membrane down their concentration or electrochemical gradient, without requiring cellular energy. Examples include the diffusion of water and the movement of certain ions along an electrical gradient.
Active Transport: This involves the movement of substances across the tubular membrane against their concentration or electrochemical gradient, requiring the expenditure of cellular energy (usually ATP). Active transport often involves carrier proteins that bind to the substance and facilitate its movement across the membrane. Examples include the reabsorption of glucose, amino acids, and certain ions like sodium.

Only 60-70% of the original filtrate reaches the loop of Henle. A significant portion of water, sodium, and chloride is reabsorbed in the loop, reducing the volume of filtrate entering the distal convoluted tubule (DCT) to 15-20% of the original amount. This dramatically changes the filtrate’s composition.

The distal convoluted tubule (DCT) reabsorbs more electrolytes, particularly sodium, making the filtrate entering the collecting ducts quite dilute.

The primary function of the collecting ducts is to reabsorb as much water as the body needs, depending on the body’s hydration state and hormonal influences.

Transport Maximum (Tm) or Renal Threshold

Active transport is mediated by carrier proteins in the epithelial membrane. These proteins have a limited capacity to bind and transport substances. The kidneys’ maximum capacity for reabsorption of a substance is known as the transport maximum (Tm) or renal threshold.

For example, the normal blood glucose level ranges from 3.5 to 8 mmol/L (63 to 144 mg/100 mL). If the blood glucose level exceeds the transport maximum (Tm) of approximately 9 mmol/L (160 mg/100 mL), glucose will appear in the urine. This occurs because all available carrier sites are occupied, and the active transport mechanism is overloaded. This condition is known as glucosuria.

Other substances reabsorbed by active transport include sodium, calcium, potassium, phosphate, and chloride.

The transport maximum, or renal threshold, of some substances varies depending on the body’s needs at a particular time. In some cases, reabsorption is regulated by hormones.

Hormonal Regulation of Selective Reabsorption

Several hormones influence selective reabsorption in the nephron:

Parathyroid Hormone (PTH): Secreted by the parathyroid glands, PTH, along with calcitonin from the thyroid gland, regulates the reabsorption of calcium and phosphate in the distal convoluted tubules and collecting ducts. PTH increases blood calcium levels, while calcitonin lowers them.
Antidiuretic Hormone (ADH) (Vasopressin): Secreted by the posterior pituitary, ADH increases the permeability of the distal convoluted tubules and collecting ducts to water, enhancing water reabsorption. ADH secretion is controlled by a negative feedback system that responds to changes in blood osmolarity and blood volume.
Aldosterone: Secreted by the adrenal cortex, aldosterone increases the reabsorption of sodium and water and the excretion of potassium in the distal convoluted tubules and collecting ducts. Aldosterone secretion is regulated through the renin-angiotensin-aldosterone system (RAAS), a negative feedback system that responds to changes in blood pressure and sodium levels.
Atrial Natriuretic Peptide (ANP): Secreted by the atria of the heart in response to stretching of the atrial walls when blood volume increases, ANP decreases reabsorption of sodium and water in the proximal convoluted tubules and collecting ducts. ANP secretion is also regulated by a negative feedback system.

Tubular Secretion

Tubular secretion is the process by which substances are transported from the peritubular capillaries into the filtrate within the tubules.

Filtration occurs as blood flows through the glomerulus, but some substances may not be entirely filtered out of the blood due to the short time blood spends in the glomerulus.

Substances not required by the body and foreign materials, such as drugs like penicillin and aspirin, are cleared from the blood through tubular secretion.

Tubular secretion of hydrogen ions (H+) is crucial for maintaining normal blood pH by removing excess acid from the body.

Composition of Urine

Appearance: Urine is typically clear and amber in color. The amber hue is due to the presence of urobilin, a bile pigment that is altered in the intestine, reabsorbed into the bloodstream, and then excreted by the kidneys.
Specific Gravity: The specific gravity of urine ranges between 1.020 and 1.030. Specific gravity is a measure of the concentration of solutes in the urine.
pH: The pH of urine is around 6, but the normal range is 4.5-8. This indicates that urine is typically slightly acidic.

Daily Volume and Variability:

A healthy adult passes 1000 to 1500 mL of urine per day.
The volume of urine produced and its specific gravity vary depending on fluid intake and the amount of solutes excreted.

Constituents of Urine:

Urine consists primarily of water, but it also contains various solutes. The approximate composition is:

Water: 96%
Urea: 2% (primary nitrogenous waste product of protein metabolism)
Other Solutes (2%):

Uric acid
Creatinine
Ammonia
Sodium
Potassium
Chlorides
Phosphates
Sulfates
Oxalates

Renin-Angiotensin-Aldosterone System (RAAS)

The RAAS is a critical hormonal system that regulates blood pressure, blood volume, and electrolyte balance (primarily sodium and potassium). Aldosterone, a hormone produced by the adrenal cortex, plays a key role in regulating sodium excretion in the urine.

Step-by-step breakdown of the RAAS:

Renin Release: Specialized cells in the afferent arteriole of the nephron (juxtaglomerular cells) release the enzyme renin into the bloodstream. Renin release is triggered by:

Sympathetic nervous system stimulation
Low blood volume
Low arterial blood pressure

Angiotensinogen Conversion: Renin acts on angiotensinogen, a plasma protein produced by the liver. Renin converts angiotensinogen into angiotensin I.

Angiotensin-Converting Enzyme (ACE): Angiotensin-converting enzyme (ACE) is an enzyme primarily found in the lungs (but also in the proximal convoluted tubules and other tissues). ACE converts angiotensin I into angiotensin II.

Angiotensin II Effects:

Angiotensin II is a potent vasoconstrictor: It causes the blood vessels to constrict, which increases blood pressure.
Aldosterone Release: Angiotensin II stimulates the adrenal cortex to secrete aldosterone. Elevated blood potassium levels also stimulate aldosterone secretion.
Sodium and Water Reabsorption: Aldosterone acts on the distal convoluted tubules and collecting ducts of the nephron to increase sodium reabsorption from the filtrate back into the bloodstream. Water follows sodium due to osmosis, so water reabsorption also increases.
Blood Volume Increase: Increased sodium and water reabsorption leads to an increase in blood volume.

Negative Feedback: The increase in blood volume and blood pressure caused by the RAAS has a negative feedback effect:

It reduces renin secretion from the juxtaglomerular cells, shutting down the RAAS pathway.

Additional Points about the RAAS:

Potassium Balance: When aldosterone increases sodium reabsorption, it also increases potassium excretion in the urine. This is an important mechanism for maintaining potassium balance in the body. Elevated blood potassium levels directly stimulate aldosterone secretion, leading to potassium excretion.
Hypokalemia: Profound diuresis (excessive urine production) can lead to hypokalemia (low blood potassium levels) because of increased potassium excretion.

Electrolyte Balance

Changes in the concentration of electrolytes in the body fluids may be due to changes in:

The body water content, or
Electrolyte levels.
Several mechanisms maintain the balance between water and electrolyte concentration.

Calcium Balance

The regulation of calcium levels in the body is maintained by the combined actions of:

Parathyroid Hormone (PTH): Secreted by the parathyroid glands, PTH increases blood calcium levels by:

Stimulating the release of calcium from bone.
Increasing calcium reabsorption in the kidneys.
Indirectly increasing calcium absorption in the intestines (by activating vitamin D).

Calcitonin: Secreted by the thyroid gland, calcitonin lowers blood calcium levels by:

Inhibiting the release of calcium from bone.
Increasing calcium excretion in the kidneys.

Organs of the Urinary Tract

Ureters
Urinary bladder
Urethra

URETERS

The ureters are tubes that transport urine from the kidneys to the urinary bladder. They are approximately 25-30 cm long and have a diameter of about 3 mm.

The ureter is continuous with the funnel-shaped renal pelvis. It travels downward through the abdominal cavity, situated behind the peritoneum and in front of the psoas muscle. It then enters the pelvic cavity and passes obliquely through the posterior wall of the bladder.

Ureteral Anti-Reflux Mechanism:

The oblique passage of the ureters through the bladder wall is crucial. As urine accumulates and the pressure within the bladder rises, the ureters are compressed, effectively closing the openings into the bladder.
This arrangement prevents the backflow (reflux) of urine into the ureters (toward the kidneys) both as the bladder fills and during micturition (urination), when the muscular bladder wall contracts and pressure increases.

Ureter Structure:

The walls of the ureters are composed of three layers of tissue:

Outer Layer (Fibrous Tissue): An outer covering of fibrous tissue. Continuous with the fibrous capsule of the kidney.
Middle Layer (Muscular Layer): Consists of interlacing smooth muscle fibers that form a functional unit around the ureter. An additional outer longitudinal layer is present in the lower third of the ureter.
Inner Layer (Mucosa): Composed of transitional epithelium (urothelium). This type of epithelium is designed to stretch and accommodate changes in volume.

Ureter Function:

Peristalsis: Peristalsis is an inherent property of the smooth muscle layer. It involves rhythmic contractions that propel urine along the ureter.
Peristaltic Waves: Peristaltic waves occur several times per minute, increasing in frequency with the volume of urine produced. These waves send small spurts of urine along the ureter towards the bladder.

URINARY BLADDER

The urinary bladder serves as a reservoir for urine storage. It is situated in the pelvic cavity. Its size and position vary depending on the volume of urine it contains. When distended (full), the bladder rises into the abdominal cavity.

Urinary Bladder Structure:

Shape: The bladder is roughly pear-shaped when empty, but it becomes more balloon-shaped as it fills with urine.
Base and Neck: The posterior surface is the base. The bladder opens into the urethra at its lowest point, the neck.
Peritoneum: The peritoneum covers only the superior surface of the bladder before it turns upward as the parietal peritoneum, lining the anterior abdominal wall. Posteriorly, it surrounds the uterus in females and the rectum in males.

The bladder wall is composed of three layers:

Outer Layer (Connective Tissue): A layer of loose connective tissue that contains blood vessels, lymphatic vessels, and nerves. The upper surface is covered by the peritoneum.
Middle Layer (Detrusor Muscle): Consists of interlacing smooth muscle fibers and elastic tissue arranged loosely in three layers. This muscle is called the detrusor muscle. When it contracts, it empties the bladder.
Inner Layer (Mucosa): Composed of transitional epithelium. This epithelium readily permits distension of the bladder as it fills. When the bladder is empty, the inner lining is arranged in folds, or rugae, which gradually disappear as the bladder fills.

Bladder Capacity and Sensation: The bladder is distensible, but as it fills, awareness of the need to urinate is felt. The total capacity is rarely more than about 600 mL.

Trigone: The three orifices (openings) in the bladder wall form a triangle or trigone:

The upper two orifices on the posterior wall are the openings of the ureters.
The lower orifice is the opening into the urethra.

Internal Urethral Sphincter:

The internal urethral sphincter is a thickening of the urethral smooth muscle layer in the upper part of the urethra, it controls outflow of urine from the bladder. This sphincter is under involuntary control.

URETHRA

The urethra is the canal that extends from the neck of the bladder to the external urethral orifice, allowing urine to exit the body.

Length Difference (Male vs. Female): The urethra is significantly longer in males than in females.
Male Urethra: The male urethra serves dual functions: urinary and reproductive, as it transports both urine and semen.

Female Urethra:

Length and Diameter: The female urethra is approximately 4 cm long and 6 mm in diameter.
Location: It runs downward and forward behind the symphysis pubis.
External Urethral Orifice: It opens at the external urethral orifice, located just in front of the vagina.
External Urethral Sphincter: The external urethral orifice is guarded by the external urethral sphincter, which is under voluntary control.

Female Urethra Structure:

Layers: The wall of the female urethra has two main layers:

Outer Muscle Layer:

Smooth Muscle: An inner layer of smooth muscle, which is under autonomic (involuntary) nerve control.
Striated Muscle: An outer layer of striated (skeletal/voluntary) muscle surrounding the smooth muscle. This forms the external urethral sphincter.

Inner Mucosa:

An inner lining of mucosa that is continuous with the mucosa of the bladder.
Supported by loose fibroelastic connective tissue containing blood vessels and nerves.
Epithelium: Proximally (near the bladder), it consists of transitional epithelium (urothelium). Distally (near the external orifice), it is composed of stratified squamous epithelium.

Micturition (Urination)

Micturition is the process of emptying the urinary bladder.

Infants:

Stretch Receptors: Accumulation of urine in the bladder activates stretch receptors in the bladder wall.
Afferent Impulses: These receptors generate sensory (afferent) impulses that are transmitted to the spinal cord.
Spinal Reflex: A spinal reflex is initiated in the spinal cord.
Detrusor Muscle Contraction: This stimulates involuntary contraction of the detrusor muscle (the bladder wall muscle).
Internal Sphincter Relaxation: Simultaneously, there is relaxation of the internal urethral sphincter.
Urine Expulsion: This results in the expulsion of urine from the bladder.

Developed Bladder Control (Adults):

Micturition Reflex Stimulation: The micturition reflex is still stimulated as the bladder fills.
Ascending Sensory Impulses: However, sensory impulses also pass upward to the brain, leading to an awareness of the need to urinate (typically around 300-400 mL in adults).
Voluntary Control: Through learned and conscious effort, contraction of the external urethral sphincter and the muscles of the pelvic floor can inhibit micturition until it is convenient to urinate.

Assisted Urination: Urination can be assisted by increasing pressure within the pelvic cavity. This is achieved by lowering the diaphragm and contracting the abdominal muscles.
Overdistension: Overdistension of the bladder is extremely painful. In this state, there is a tendency for involuntary relaxation of the external sphincter to occur, allowing a small amount of urine to escape (provided there is no mechanical obstruction).

The Effects of Aging on the Urinary System

Aging brings about several changes in the urinary system:

Kidney Function:

Nephron Decline: The number of nephrons declines with age.
Glomerular Filtration Rate (GFR) Decrease: The glomerular filtration rate (GFR) falls, meaning the kidneys filter blood less efficiently.
Tubular Function Decline: The renal tubules function less efficiently.
Concentration Impairment: The kidneys become less able to concentrate urine. This makes older adults more susceptible to fluid balance issues, such as dehydration or fluid overload.
Drug Elimination: Elimination of drugs also becomes less efficient, potentially leading to drug accumulation and toxicity.

Bladder Function:

Urinary Frequency and Urgency(Detrusor Muscle Control Decline): The decreased control over the detrusor muscle often results in an urgent need to urinate and increased urinary frequency.
Nocturia: Nocturia (the need to urinate frequently during the night) becomes increasingly common in older adults.
Incontinence: Incontinence (the involuntary leakage of urine) is more prevalent in older adults, affecting a significant percentage of both men and women. These numbers tend to double as individuals reach advanced ages (85 years+).

Prostate Enlargement (Males):

Benign Prostatic Hyperplasia (BPH): Enlargement of the prostate gland (benign prostatic hyperplasia or BPH) is common in older men.
Urinary Retention: BPH can cause retention of urine (difficulty completely emptying the bladder).
Micturition Problems: It can also lead to various problems with micturition, such as a weak urine stream, straining to urinate, and frequent urination.

Nursing Lecture Notes - The Urinary System

Common Deviations from Normal Structure and Function (Disorders)

When parts of the urinary system are not working normally, it can lead to a range of problems affecting waste removal, fluid balance, and urination.

Diseases of the Kidneys:

Glomerulonephritis (GN): Inflammation or damage to the glomeruli (the filters in the nephrons). This can be caused by infections or autoimmune reactions. Damaged glomeruli may leak protein and blood into the urine (proteinuria and haematuria), and their filtering ability is reduced. Severe or chronic GN can lead to renal failure.

Nephrotic Syndrome: Not a disease itself, but a set of symptoms (syndrome) caused by significant damage to the glomeruli, often due to GN or other conditions.

Features: Large amounts of protein in the urine (marked proteinuria), low protein levels in the blood (hypoalbuminaemia), and widespread swelling (generalised oedema) due to fluid imbalance caused by low blood protein. Also high levels of fats in the blood.

Diabetic Nephropathy: Kidney damage caused by diabetes mellitus. High blood sugar levels over time damage the blood vessels in the kidneys, especially the glomeruli. This leads to reduced kidney function and can progress to renal failure. Hypertension often worsens this condition.

Hypertension and the Kidneys: High blood pressure can damage the small blood vessels in the kidneys, leading to reduced kidney function. Kidney disease can also cause or worsen high blood pressure (secondary hypertension).

Kidney Infections (Pyelonephritis): Infection of the renal pelvis and kidney tissue, usually caused by bacteria travelling up from the bladder and ureters. Causes fever, loin pain, and can damage kidney tissue if not treated, potentially leading to chronic renal failure.

Renal Failure (Kidney Failure): Occurs when the kidneys lose their ability to filter blood and perform their functions.

Acute Renal Failure: A sudden loss of kidney function. Can be caused by severe shock (reduced blood flow), toxins, or blockage of urine outflow. Often reversible with treatment.
Chronic Renal Failure (Chronic Kidney Disease - CKD): A gradual, progressive loss of kidney function over time. Common causes include diabetes, hypertension, and chronic GN. It is often silent in early stages but leads to a build-up of waste products in the blood (uraemia), fluid imbalance, anaemia, and other problems as kidney function declines.

Renal Calculi (Kidney Stones): Hard deposits that form in the kidneys from substances in the urine. They can range in size. Small stones may pass out in urine, but larger ones can get stuck in the ureter or block urine outflow, causing severe pain (renal colic), damage to the urinary tract lining, infection, and potentially kidney damage if they block urine flow for a long time.

Congenital Abnormalities: Problems with kidney development before birth, like a kidney located in the wrong place (misplaced/ectopic kidney) or polycystic kidney disease (cysts form in the kidneys, leading to damage and failure over time).

Kidney Tumours: Abnormal growths in the kidney. Can be benign or malignant. Renal adenocarcinoma is a common type of malignant kidney tumour in adults, often found in older males. It can spread locally and to distant sites.

Diseases of the Renal Pelvis, Ureters, Bladder and Urethra:

Obstruction to Urine Outflow: Blockages anywhere in the urinary tract below the kidneys prevent urine from flowing out.

Causes: Kidney stones, tumours pressing on the ureters or bladder, enlarged prostate gland (in males), or strictures (narrowing) of the ureters or urethra.
Effects: Urine backs up, causing swelling of the renal pelvis and ureters (hydronephrosis and hydroureter). This pressure can damage kidney tissue over time. Obstruction also increases the risk of infection.

Urinary Tract Infections (UTIs): Infections in any part of the urinary tract, most commonly the bladder (cystitis). Usually caused by bacteria entering the urethra, often from the bowel. Infections can spread upwards to the ureters (ureteritis) and kidneys (pyelonephritis). Symptoms include pain/burning on urination (dysuria), frequent urination, and cloudy urine. UTIs are more common in females due to a shorter urethra.

Tumours of the Bladder: Abnormal growths in the bladder lining. Can be benign or malignant. Often cause painless bleeding in the urine (haematuria). Bladder cancer is linked to smoking and industrial chemicals.

Urinary Incontinence: Involuntary loss of urine. This means urine leaks out without the person consciously controlling it.

Causes: Weakness of the pelvic floor muscles (e.g., after childbirth, ageing - stress incontinence), problems with bladder muscle control (e.g., in UTIs, tumours - urge incontinence), or incomplete emptying of the bladder causing overflow (e.g., enlarged prostate, nerve damage).

Understanding the structure and function of the urinary system, and how these can deviate, is crucial for providing care related to fluid balance, waste removal, and urination problems.

Revision Questions for Page 7 (Urinary System):

What is the main function of the urinary system?
List the four main parts of the urinary system.
Describe the location and gross structure of the kidneys.
What is a nephron and what is its main function? Name its main parts.
Explain the three main processes involved in urine formation in the nephron.
Where do filtration, selective reabsorption, and secretion primarily occur in the nephron?
How do the kidneys help maintain the body's water balance? Mention the main hormone involved.
How do the kidneys help maintain the body's electrolyte balance? Mention the main hormones involved.
What is the main function of the ureters?
What is the main function of the urinary bladder?
Describe the process of micturition (urination), mentioning the roles of the bladder muscle and sphincters.
List three ways the urinary system changes as a person gets older.
What is glomerulonephritis? What are some common symptoms?
What is nephrotic syndrome? Describe its main features.
What is renal failure? Briefly explain the difference between acute and chronic renal failure.
What are kidney stones (renal calculi)? What problems can they cause?
What is a urinary tract infection (UTI)? Why are UTIs more common in females?
What is urinary incontinence? Mention two potential causes.

References:

Cohen, JB and Hull, L.K (2016) Memmlers – The Human body in Health and diseases 13th Edition, Wolters, Kluwer.
Scott, N.W. (2011) Anatomy and Physiology made incredibly easy. 1st Edition. Wolters Kluwers, Lippincotts Williams and Wilkins.
Moore, L. K, Agur, M.R.A and Dailey, F.A. (2015) Essential Clinical Anatomy.15th Edition. Wolters Kluwer.
Cohen, J.B and Hull, L.K (2016) Memmler's Structure and Function of the Human Body. 11th Edition. Wolters Kluwer, China
Snell, S. R. (2012) Clinical Anatomy by Regions. 9th Edition. Wolters Kluwer, Lippincott Williams and Wilkins, China
Wingerd, B, (2014) The Human Body-Concepts of Anatomy and Physiology. 3rd Edition Lippincott Williams and Wilkins and Wolters Kluwer.
Rohen, Y.H-Orecoll. (2015) Anatomy.A Photographic Atlas 8th Edition. Lippincott Williams & Wilkins.
Waugh, A., & Grant, A. (2014). Ross and Wilson Anatomy & Physiology in Health and Illness (12th ed.). Churchill Livingstone Elsevier.

Notes prepared by: Nurses Revision

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