Module 3:

Management of Cardiovascular
Diseases, Sickle Cell Disease (SCD) &
Chronic Kidney Disease
 EPIDEMIOLOGY OF CARDIOVASCULAR
DISEASES
Definition of Cardiovascular Diseases
• Cardiovascular diseases (CVDs) are a group of disorders predominantly
affecting the heart and blood vessels and include:

– Coronary heart disease – disease of the blood vessels supplying the heart
muscle

– Cerebrovascular disease - disease of the blood vessels supplying the brain

– Peripheral arterial disease – disease of blood vessels supplying the arms and
legs

– Disease of the heart valve – rheumatic heart disease (RHD), and congenital
heart disease
 Burden of Cardiovascular Diseases
• Cardiovascular diseases (CVDs) are the number one cause of death globally

• An estimated 17.9 million people died from CVDs in 2016, representing 31% of all
global deaths. Of these deaths, 85% are due to heart attack and stroke

• Over three-quarters of CVD deaths take place in low- and middle-income countries

• Out of the 17 million premature deaths (under the age of 70) due to
noncommunicable diseases in 2015, 82% are in low- and middle-income countries,
and 37% are caused by CVDs(1,2)

• By 2030, almost 23.6 million people will die from CVDs, mainly from heart disease
and stroke

– These are projected to remain the single leading causes of death

Distribution of Major Causes of Death
Including CVDs
Distribution of Global NCD by Cause of
Death
Distribution of CVD Deaths Due to Heart Attacks,
Strokes, and Other Types of CVD Diseases - Males
 Distribution of CVD Deaths due to Heart Attacks,
Strokes, and other Types of CVD Diseases - Females
Current Status of CVD and NCDs in Tanzania
 Risk Factors for Cardiovascular Disease
• The most important behavioural risk factors of heart disease and stroke are
unhealthy diet, physical inactivity, and tobacco use

• Behavioural risk factors are responsible for about 80% of coronary heart disease
and cerebrovascular disease

• Tobacco is the leading global cause of preventable death and kills nearly 6 million
people each year

• Majority of these premature deaths occurring among people living in low- and
middle-income countries
• Tobacco kills one in two of its long-term users
• More deaths are caused each year by tobacco use than by the combined number
of deaths from Human immunodeficiency virus (HIV), illegal drug use, alcohol use,
motor vehicle injuries, suicides, and murders combined
• Estimating a 10-year risk of getting a CVD

– From the below chart, we can work out one’s 10-risk of getting a CVD

– It helps predict the risk over 10 years of heart attack, stroke, or death
from cardiovascular disease

– It comprises of age, sex, diabetes history, blood pressure level, and

smoking habit

– For instance, a 70 years old diabetic, non – hypertensive, smoker

male has a 20 – 30 % risk
 Prevention of Cardiovascular Diseases
• Prevention of CAD can be divided as follows: primodial, primary,
and secondary preventions
– Preventive measures of NCDs/CVDs includes lifestyle modifications
• Primodial prevention: This prevention directed towards
discouraging the children from adapting harmful lifestyle such as:
smoking, eating pattern, physical exercise, alcoholism
• Primary prevention: This consists of the elimination of its
modifications of risk factors of disease, with the following approach
– Population strategy: Dietary changes: Consumption of saturated fats
should be less than 10% of total energy intake
– Identifying the at-risk group persons for CAD and providing preventive
care
– Individuals with hypertension are given treatment
– smokers to give up smoking
• Secondary prevention: prevention of reoccurrence of CAD by
cessation of smoking, and regularly taking tablets is the focus
 Prevention of ARF/RHD
• Levels of prevention:

– PRIMORDIAL: Control environmental risk factors

– PRIMARY: Appropriate treatment of acute pharyngitis and if has

ARF give Aspirin 80mg/kg, bed rest

– SECONDARY: Monthly Benzanthine penicillin 2.4Mu

– TERTIARY: Management of complications like heart failure,

pulmonary hypertension, atrial and ventricular arrythmias,
infective endocarditis
 Key Points
• Cardiovascular diseases (CVDs) are a group of disorders predominantly
affecting the heart and blood vessels

• More people die annually from CVDs than from any other cause

• An estimated 17.9 million people died from CVDs in 2016, representing

31% of all global deaths. Of these deaths, 85% are due to heart attack
and stroke

• Risk factors of heart disease and stroke include unhealthy diet, physical
inactivity, and tobacco use

• Prevention of CVD include primordial, primary, secondary prevention

 Session Evaluation
• What is the burden of cardiovascular
diseases?

• What are the risk factors for cardiovascular

diseases?

• How do you prevent cardiovascular diseases?

CLINICAL PRESENTATION OF PATIENTS WITH
CARDIOVASCULAR DISEASES
• Symptoms of Heart Attacks and Strokes
– Often, there are no symptoms of the underlying
disease of the Heart and blood vessels

– A heart attack or stroke may be the first warning

of underlying disease
Symptoms of a Heart Attack/acute coronary
syndrome
• Pain or discomfort in the centre of the chest

• Pain or discomfort in the arms, the left shoulder, elbows, jaw, or back

• The person may experience difficulty in breathing or shortness of breath

• Feeling sick or vomiting

• Feeling light-headed or faint

• Breaking into a cold sweat

• Becoming pale

• Women are more likely to have shortness of breath, nausea, vomiting, and back or jaw
pain
 Symptoms of a Stroke
• The most common symptom of a stroke is:

• Sudden weakness of the face, arm, or leg

• Most often on one side of the body
• Other symptoms include sudden onset of:

– Numbness of the face, arm, or leg, especially on one side of the body
– Confusion
– Difficulty speaking or understanding speech
– Difficulty seeing with one or both eyes
• Other symptoms include sudden onset of:

– Difficulty walking
– Dizziness
– Loss of balance or coordination
– Severe headache with no known cause
– Fainting or unconsciousness
Spot a Stroke: Signs and Symptoms
Clinical Manifestations of Acute Rheumatic
Fever (ARF)
• Acute rheumatic fever commonly presents as
a constellation of symptoms such as sore
throat, fever, joints pain, chest pain, and skin
changes while rheumatic heart disease will
present mainly with features of disease
complications
 Major Manifestations of Acute Rheumatic
Fever
• Major Manifestations

– Carditis

– Polyarthritis

– Chorea

– Erythema marginatum

– Subcutaneous nodules
• Minor Manifestations

– Arthralgia

– Fever, malaise, anorexia

– ESR>60

– CRP>3

– Prolonged PR on ECG
 Key Points
• Common symptoms and signs of patients with cardiovascular
diseases:

– In cases of heart attack patients will experience pain or discomfort in the

centre of the chest, pain or discomfort in the arms, the left shoulder,
elbows, jaw, or back
• The person may experience difficulty in breathing or shortness of breath
– In cases of stroke, the patient may experience difficulty in:
• speaking or understanding speech
• seeing with one or both eyes
• walking and dizziness
– In cases of rheumatic heart disease the patient may experience sore
throat, fever, joints pain, chest pain, and skin changes while rheumatic
heart disease will present mainly with features of disease complications
 MANAGEMENT OF PATIENTS WITH
HYPERTENSION
• Learning Objectives
• At the end of this session participants are expected to be able to:

– Explain factors affecting blood pressure (BP)

– Describe diagnosis and classification of hypertension

– Recognize common symptoms and signs of hypertension

– Identify complications of hypertension

– Perform appropriate investigations for hypertension

– Provide pharmacological and non-pharmacological treatment of hypertension

– Manage hypertensive emergency, heart attack (ACS) and heart failure

– Implement referral pathway for hypertension

– Conduct regular follow up monitoring to patients with hypertension

 Factors Affecting Blood Pressure
• Physiological factors include:

– Age: tends to increase in elder people

– Sex: before the onset of menopause women have a little lower BP than that of males of the same age
group, after menopause, women have a little higher BP than that of males

– Meals: after meals, BP is higher

– Emotion: range and panic may rise BP

– Exposure to cold: increase BP in order to preserve body heat, the body tries to keep temperature by
cutaneous vasoconstriction as a result of SNS stimulation

– Exercise

– Sleep: cause a fall in BP

– Circadian rhythm: BP is highest in the morning and least in the night

 Pathological Factors
• Pathological Factors Include:

– Clinical conditions that alter BP include renal artery

stenosis, pheochromacytoma, and pre-eclampsia

– Drug-induced: sympathetic stimulants like

adrenaline, noradrenaline, and phenylephrine cause
rise of BP, while vascular smooth muscle relaxants
like hydralazine reduces BP
 Types of Hypertension
• There are two types of high blood pressure:

– Primary (essential) hypertension

– Secondary hypertension
 Primary (Essential) Hypertension
• For most adults, there is no identifiable cause of high blood
pressure

• This type of high blood pressure, called primary (essential)

hypertension, tends to develop gradually over many years

• Primary (essential) hypertension is the most common form of

hypertension, accounting for 90–95% of all cases of hypertension

• Insulin resistance, which is common in obesity and is a component

of syndrome X (or the metabolic syndrome), is also thought to
contribute to hypertension
 Risk Factors for Primary Hypertension
 Age: Systolic BP increase progressively with increasing age

 Alcohol

 Cigarette smoking

 Diabetes: hypertension is more common in diabetes mellitus

 Elevated serum lipids: a primary risk factor for atherosclerosis

 Excess dietary sodium: contributes to hypertension

 Gender: Hypertension is more prevalent in young male adults, but after 55 years, more prevalent in
women

 Family history of hypertension

 Obesity

 Sedentary lifestyle: Regular physical activity reduces obesity and decreases BP

 Stress: Increase the incidence of hypertension

 Secondary Hypertension
• Secondary hypertension results from an identifiable cause.

• Renal disease is the most common secondary cause of hypertension

• Hypertension can also be caused by endocrine conditions such as:

• Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly,

Conn's syndrome or hyperaldosteronism, hyperparathyroidism and
pheochromocytoma, chronic kidney disease, renovascular disease,
coarctation of the aorta, Takayasu Arteritis, drug-induced or drug-
related (e.g. chronic steroid therapy)
 Diagnosis of Hypertension
• Diagnosis of hypertension is made based on three
different elevated systolic readings of ³ 140 mmHg
and/or diastolic readings ³ 90mmHg.

• It requires three BP measurements within a week.

• Prevalence of HTN in LMICs is high, being driven by the

increase in CVD risk factors.

• It is a silent killer but can be controlled.

Correct Blood Pressure Measurement
 Measuring Blood Pressure
• Measuring blood pressure is the only way to diagnose hypertension, as most
people with raised blood pressure have no symptoms

• Effective treatment algorithms for hypertension are dependent on accurate

blood pressure measurement

• The following advice should be followed for measuring blood pressure:

• Use the appropriate cuff size, noting the lines on the cuff to ensure that it is
positioned correctly on the arm
• If the arm circumference is > 32cm, use a large cuff
• It is preferable to measure blood pressure in both arms and use the arm with
the higher reading thereafter, this may not be practical in a busy primary
care environment
Blood Pressure Levels in Children
• These readings represent the lower limits for
abnormal blood pressure readings according
to age and gender.

• Any reading greater to or equal to these

readings require further evaluation by a
physician.
 Common Symptoms and Signs of
Hypertension
• Hypertension is usually symptomless. However, patients may present with
symptoms of complications.

• Headaches - Headaches may be experienced due to an elevation in blood

pressure.

• Sometimes morning headaches can also be due to hypertension.

• Dizziness - Dizziness is often experienced by people with high blood

pressure.

• However, dizziness cannot always be treated as a symptom of hypertension.

• If dizziness is experienced it is always wise to consult a medical practitioner.
• Heart pain
• Palpitations

• Nosebleeds - Nosebleeds without particular reason might be a symptom of high blood

pressure

• It is better to check the blood pressure in such cases

• Difficulty in breathing

• Tinnitus (ringing or buzzing in the ears)

• Blurred Vision

• Frequent urination

• Hypertension may be suspected on the basis of the presence of hypertensive retinopathy

detected by examination of the optic fundus found in the back of the eye using
ophthalmoscopy
 Complications of Hypertension
• Hypertension is the most important preventable risk factor for:

– Premature death
– Ischemic heart disease
– Strokes
– Peripheral vascular disease
– Other cardiovascular diseases including heart failure, aortic aneurysms, diffuse
atherosclerosis, and pulmonary embolism
• Hypertension is also a risk factor for cognitive impairment and dementia,
and chronic kidney disease

• Other complications include: hypertensive retinopathy and hypertensive

nephropathy, nephrosclerosis, hypertensive encephalopathy, and
bleeding from the aorta
 Hypertensive Emergency
• Severely elevated blood pressure (equal to or greater than a systolic 180
or diastolic of 110, sometimes termed malignant or accelerated
hypertension, is referred to as a "hypertensive crisis".

• People with blood pressure in this range may have no symptoms but are
more likely to report headaches (22% of cases) and dizziness than the
general population and may have visual deterioration or breathlessness
due to heart failure or a general feeling of malaise due to renal failure.

• There is evidence of direct damage to one or more organs as a result of

the severely elevated blood pressure which may include hypertensive
encephalopathy, altered level of consciousness, retinal papilloedema,
chest pain (myocardial infarction), aortic dissection, signs of pulmonary
oedema, and deterioration of kidney function.
 Investigations for Hypertension
• Laboratory Tests

– Renal

• Microscopic urinalysis, proteinuria, BUN and/or creatinine

– Endocrine

• Serum sodium, potassium, calcium, TSH

– Metabolic

• Fasting blood glucose, HDL, LDL, and total cholesterol, triglycerides

– Others

• Electrocardiogram
• Echo cardiography
 Management of Hypertension
• The primary goal of therapy of hypertension should be

– effective control of BP in order to prevent, reverse or delay the progression of

complications and
• thus reduce the overall risk of an individual without adversely affecting the quality of
life.
• Patients should be explained that the lifestyle modifications and drug
treatment is generally lifelong and regular drug compliance is important.

• For most patients, blood pressure is considered controlled when SBP <
140 mmHg and DBP < 90 mmHg.

• For patients with diabetes or a high risk of CVD, certain guidelines

recommend lower targets: SBP < 130 mmHg and DBP < 80 mmHg.
Non-Pharmacological Interventions
• Prevention interventions:

– Maintain normal body weight for adults (e.g. body mass index 20–25 kg/m2).
– Reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day).
– Engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most days of the
week).
• Limit alcohol consumption to no more than 2 units/day in men and no more than 1 units/day in
women.

• Consume a diet rich in fruit and vegetables (e.g. at least five portions per day).

• Effective lifestyle modification may lower blood pressure.

• Lifestyle counselling (on a healthy diet, physical activity, the harms of tobacco use, and harmful
use of alcohol) is a critical component of good hypertension management

– It is often recommended as a first step for patients with blood pressure of SBP 130–139 mmHg and /or
DBP 80–89 mmHg who do not have other CVD risk factors
 Pharmacological Interventions
• •There are four main classes of antihypertensive
medications:

– Angiotensin converting enzyme (ACE) inhibitors.

– Angiotensin receptor blockers (ARB).

– Calcium channel blockers (CCB).

– Thiazide and thiazide-like diuretics.

 Hypertensive Emergency
• SBP 180 mmHg and or DBP 110 mmHg PLUS target end organ
damage and symptoms such as headache, visual disturbances,
shortness of breath, chest pain

– I.V medications preferable such as Esmolol and Labeterol,

nitroglycerine infusion
– In case of pregnancy I.V hydralazine
– Emergency referral
• SBP 180 mmHg and or DBP 110 mmHg WITHOUT features for
target end organ damage

– Commence oral medications

 Acute Coronary Syndrome (ACS) (Heart
Attack)
• Do resting 12 lead ECG if available.

• Give ASA 300mg and clopidogrel 600mg.

• Give Statins; atorvastatin 80 mg or Rosuvastin

40mg.

• Timely referral to PCI/THROMBOLYTIC CENTER

(the role of ambulance).
 Heart Failure Patient
• Patients in acute heart failure should
immediately be referred to the hospital for
further management.

• Give Lasix intravenously or per oral 40 mg.

 Lipid Control
• Lipid-lowering drugs

– Statins Atorvastatin or Simvastatin 20mg daily (max 40mg).

– If cholesterol (LDL) remains high after 3 months, then refer/treat.

– If fasting triglycerides > 1.7mmol/l),

– Add fenofibrate or clofibrate. Or

– If only triglyceride raised then fibrate alone (without a statin).

 Follow up Patients with Hypertension
• What to do at every visit:

– Ask patient to check BP regularly at a nearby health facility

(e.g. Once a week, and record in his/her notebook until the
next clinic appointment in approximately one month)

– If continuing BP > 160/100 mmHg despite lifestyle changes,

adherence to antihypertensive drug therapy, and good
quality BP monitoring (many BP recordings done correctly)

• refer to the HTN clinic in the hospital

• At every visit, ASK:

– How are you feeling? (in general +specific symptoms)

– How have your BP measurements been since the last control (ask
for the patients notebook)

– Lifestyle regarding tobacco, physical activity, diet

(fruits/vegetables, salt, cooking oil)

– Have you been able to follow the advices given regarding lifestyle
changes?
• At every visit, ASK:

– Do you take medication as prescribed?

– When did you last take your medicine(s)?

– Have you noticed any side effects to the treatment?

– Are there any things, in particular, you find difficult regarding following
advice given/do you not feel comfortable doing?

– (Assess compliance to treatment) Do you have any questions to your

condition or the treatment recommended?
• What to do at every visit:

– If BP, in general, is <140/90 mmHg, continue treatment as usual, also if BP in the

clinic is higher.

– If prescribed treatment is not followed investigate this instead of

adding/continuing the prescription. Address the underlying reasons for poor
adherence to treatment.

– If the patient has stopped medication some days before the clinic appointment
it is expected that BP is high and you cannot evaluate the effect of the
treatment that was prescribed at the previous visit.

– Educate the patient on why not to stop the medication before coming to the
clinic, and to do BP measurements regularly and record in the notebook.
• What to do at every visit:

– If side-effects of drugs is disturbing, change to another

drug.

– If BP is continually high despite following to treatment, add

anti-HTN drug/increase dosage. (Rather to add a second
medicine than increase one to maximum dosage)

– Remind patient to take medication every day, also on the

morning of the clinic appointment.
 Resistant Hypertension
• Resistant hypertension is defined as
hypertension that remains above goal blood
pressure in spite of concurrent use of three
antihypertensive agents belonging to different
antihypertensive drug classes.
 Key Points
• Factors affecting blood pressure are physiological and pathological:

– Physiological include age, sex, diet, and exercises.

– Pathological include diseases like kidney stenosis and eclampsia.
• There is primary and secondary hypertension.

• Treatment includes non-pharmacological and pharmacological.

• Follow up monitoring has to be done closely.

• Refer clients for further management.

 MANAGEMENT OF PATIENTS WITH STROKE
• Learning Objectives
• At the end of this session participants are expected to be able to:

– Define stroke

– Describe the burden, risks, types and causes of stroke

– Recognize the clinical presentation of stroke

– Perform appropriate investigations on patients with stroke

– Implement interventions to prevent stroke

– Provide non-pharmacological and pharmacological treatment to patients with stroke

– Implement referral pathway for patients with stroke

– Conduct regular follow-up monitoring of patients with stroke

 Definition of Stroke
• Stroke, is defined as “rapidly developing signs of focal or
global disturbance of cerebral or intracranial neuronal
function with symptoms lasting for more than 24 hours or
leading to the death of the patient with no apparent cause
other than that of vascular origin.”

• A stroke is a rapid loss of brain function due to the

disturbance in the blood supply to the brain.

• A stroke happens when blood flow to a part of the brain

stops and it is sometimes called a “brain attack.”
 Burden of Stroke
• Stroke is a leading cause of morbidity and mortality in adults in the
productive ages.

• According to the World Health Organization, each year 15 million people

suffer from stroke worldwide. Of these, 5 million die and another 5 million
are permanently disabled.

• 8% of all first-ever strokes occur in Africa and 5% of the 30 million people,

who survived stroke worldwide, live in Africa.

• Stroke is uncommon in people under 40 years; when it does occur, the main
cause is high blood pressure.

• Stroke also occurs in about 8% of children with sickle cell disease.

 Stroke mortality
• World Health Organization (WHO) estimates for 2001 indicate that death
from stroke in low-income and middle-income countries accounted for 85.5%
of stroke deaths worldwide.

• Mortality among stroke patients is highest in the first 30 days of stroke onset.

• Hospital-based studies have demonstrated a one-month mortality rate of

between 27% and 46% in Africans.

• At Muhimbili National Hospital, studies have found a 30 days mortality rate

of 33.3%.

• Stroke is a major cause of death worldwide.

 Causes of Stroke
• Stroke is uncommon in people under 40 years.

• The main cause is high blood pressure.

• Stroke also occurs in about 8% of children with

sickle cell disease.
 Types of Stroke
• There are three main types of stroke:

– Ischemic strokes

– Hemorrhagic strokes

– Transient ischemic attacks (TIAs), also referred to

as mini-strokes
 Ischemic Stroke
• Ischemic stroke is the most common form of stroke,
accounting for around 85% of strokes

• This type of stroke is caused by blockages or narrowing of

the arteries that provide blood to the brain, resulting in
ischemia - severely reduced blood flow

• These blockages are often caused by blood clots

• Clots can be caused by fatty deposits within the arteries

called plaque
 Hemorrhagic Stroke
• Hemorrhagic strokes are caused by arteries in the brain either leaking
blood or bursting open.

• The ruptures can be caused by conditions such as hypertension, trauma,

blood-thinning medications, and aneurysms (weaknesses in blood vessel
walls).

• Intracerebral haemorrhage is the most common type of hemorrhagic

stroke and occurs when brain tissue is flooded with blood after an artery in
the brain bursts.

• Subarachnoid haemorrhage is the second type of hemorrhagic stroke and

is less common: bleeding occurs in the subarachnoid space -the area
between the brain and the thin tissues that cover it.
 Transcient Ischemic Attack (TIA)
• TIAs are different from the aforementioned kinds of stroke because the flow of blood to
the brain is only briefly interrupted.

• TIAs are similar to ischemic strokes in that they are often caused by blood clots or other
debris.

• TIAs should be regarded as medical emergencies.

• They serve as warning signs for future strokes and indicate that there is a partially
blocked artery or clot source in the heart.

• According to the Centers for Disease Control and Prevention, over a third of people who
experience a TIA go on to have a major stroke within a year if they have not received any
treatment.

• Between 10-15% will have a major stroke within 3 months of a TIA.

Causes of Transient Ischemic Attacks (TIA)
Clinical Presentation of Stroke
 Symptoms of Stroke
• Strokes occur quickly and, as such, symptoms of stroke often appear suddenly without warning

• The main symptoms of stroke are as follows:

– Confusion, including trouble with speaking and understanding

– Headache, possibly with altered consciousness or vomiting
– Numbness of the face, arm or leg, particularly on one side of the body
– Trouble with seeing, in one or both eyes
– Trouble with walking, including dizziness and lack of coordination
• In addition to the persistence of the problems listed above, patients may also experience the
following:

– Bladder or bowel control problems

– Depression
– Pain in the hands and feet that gets worse with movement and temperature changes
– Paralysis or weakness on one or both sides of the body
– Trouble controlling or expressing emotions
 Diagnosis
• Strokes happen fast and will often occur
before an individual can be seen by a doctor
for a proper diagnosis.

• The acronym F.A.S.T. is a way to remember the

signs of stroke, and can help identify the onset
of stroke more quickly.
Signs of a Stroke
Stroke Recognition
 Investigations for Patients With Stroke
• There are several different types of diagnostic tests that doctors can use in order to determine
which type of stroke has occurred:

– CT scans of the brain

– Physical examination

– Blood tests

– CT scan a series of X-rays

– MRI scan

– Carotid ultrasound
– Cerebral angiogram

– Echocardiogram
• What can be done for the community

• Community to live healthier

– Avoiding smoking and second-hand smoke.

– Eating foods low in saturated fats, trans-fats, sodium, and added sugars.
– Be physically active.
– Take medicines as directed.
• Community to live healthier

– Getting blood pressure checked regularly and working with a healthcare provider to manage it if it is
high.
– Reach and maintain a healthy weight.
– Regular medical checkups.
• The acronym FAST can be used to educate the community on early recognition of stroke signs

– Face drooping: does one side of the face droop or is it numb?

– Arm weakness: is one arm weaker than the other?
– Speech difficulties: is the person unable to speak or hard to understand?
– Time for action: go to the nearest hospital
 General Measures to be Followed in all
Acute Strokes – First 48 hours
• Patient positioning

– Mild head elevation to assist venous return

– Avoid the neck being flexed
– Prevent the tongue from falling back
– No tight oxygen (O2) mask compressing the neck
veins
• Airway & Oxygen

– Pulse oximetry – target O2 saturation of >92%

– Elective intubations - for airway protection /severely
raised intracranial pressures
– May administer O2 2 – 4 litres per minute by nasal cannula

– For Patients with Chronic Obstructive Pulmonary Disease

(COPD) / Sleep Apnea, SPO2 should not be more than
92%: they need CO2 to maintain oxygen drive
• Fluids

– IV fluids - avoid Dextrose and excessive fluid

administration
– IV normal saline at 50 cc/hr if needed
• Blood sugars

– Do not give any dextrose-containing solutions

– Maintain sugars < 200 ml/L – give insulin
• Mobilization / Physiotherapy

– Bed rest for the first 24 hours

– Early gradual mobilization- (after the first 24 ours)
• Bowel

– Stool softeners
• Swallowing

– Do the Water swallowing test

• Decide on:

– Oral feeds
– Ryle’s Tub feeds
• Prevention of Bed Sore

– Frequent 2 hourly turning

– Air mattress
– DVT Prophylaxis
• Antiplatelet treatment

•In ischemic stroke start as soon as possible:

•Tabs. Junior Aspirin 300mg stat then 75mg od, plus
•Tabs Atorvastatin
• Feeding

– If prolonged tube feedings are necessary consider:

– Gastroduodenal feeding
– Percutaneous endoscopic gastrostomy PEG
– Discuss with caretakers
• Physiotherapy & Occupational therapy
programme

– A Home programme to be provided and the

primary caregiver educated
– The use of Aides and splints etc should be shown
• Primary caregiver education

– Rehabilitation-physiotherapy and occupational therapy

– Speech therapy
– Bed sore care /prevention
– Diet
– Monitoring BP/Sugars at home
– Need to continue regular medications
– Follow up in Stroke clinic
• Referral Pathway for Patients with Stroke

– Patients with acute stroke should immediately be

referred to hospital for HEAD CT SCAN.
– Don’t start antiplatelet before HEAD CT SCAN.
 Follow up Patients with Stroke
• Stroke Clinic follow up

– Give a referral slip and the necessary

investigations to be done before follow-up.
Acute care check lists
 Rehabilitation
• Strokes are life-changing events that can affect a person both physically
and emotionally, temporarily or permanently.

• After a stroke, successful recovery will often involve specific rehabilitative

activities such as:

– Speech therapy - to help with problems producing or understanding speech:

practice, relaxation, and changing communication style, using gestures or
different tones, for example, all help.
– Physical therapy - helps relearn movement and coordination.
– Occupational therapy - to improve the ability to carry out routine daily activities,
such as bathing, cooking, dressing, eating, reading & writing.
– Joining a support group - to help with common mental health problems such as
depression that can occur after a stroke.
– Support from friends/family - to provide practical support and comfort.
 Key Points
• Stroke, is defined by the World Health Organization as “rapidly developing signs of focal or
global disturbance of cerebral or intracranial neuronal function with symptoms lasting for
more than 24 hours or leading to the death of the patient with no apparent cause other than
that of vascular origin.”

• A stroke is a rapid loss of brain function due to the disturbance in the blood supply to the
brain.

• A stroke happens when blood flow to a part of the brain stops and it is sometimes called a
“brain attack.”

• There are three main types of stroke which Ischemic strokes, Hemorrhagic strokes, and
Transient ischemic attacks (TIAs), also referred to as mini-strokes.

• Treatment includes non-pharmacological and pharmacological treatment .

• Referral to be done for further management.

• Prevention includes education on healthy living and early treatment of hypertension.

• Patients have to be followed up and monitored closely.

 MANAGEMENT OF PATIENTS WITH SICKLE
CELL DISEASE
• Learning Objectives
• At the end of this session participants are expected to be able to:

– Describe sickle cell disease and types of sickle cell anaemia.

– Describe epidemiology, risk factors and pathogenesis of sickle cell disease.

– Recognize clinical presentation of sickle cell disease.

– Perform clinical and laboratory assessment of patients with sickle cell disease.

– Provide pharmacological and nonpharmacological treatment to patients with sickle cell

disease.

– Implement referral pathway for patients with sickle cell disease.

– Conduct regular follow up monitoring to patients with sickle cell.

 Definition of Sickle Cell Disease
• Sickle cell anemia is a genetic disorder whereby red blood cells
are abnormally shaped, causing problems with the flow of
blood through the body as well as the transport of oxygen
throughout the body.

• SCD is one of the disorders in a broad group of

hemoglobinopathies.

• Sickle cell anemia is an inherited disorder of hemoglobin

associated with abnormally shaped red blood cells, causing
problems with the flow of blood through the body and the
resulting transport of oxygen throughout the body.
 Hemoglobinopathie
• Hemoglobinopathies- inherited/genetic disorders that
results into abnormal production of one of the globin
chains that forms the hemoglobin.

• In SCD, the beta chain is affected by a mutation that

results into a formation of an abnormal hb called HbS.

• NB: HbS formed by a point mutation, in which glutamic

acid is substituted with valine at position 6 in the beta
hb chain gene.
 Normal Human Hemoglobin
• Normally human have the following types of hb :-

– HbA- 2alpha +2beta chains.

– HbA2- 2alpha + 2 delta chains.
– HbF- 2alpha + 2gamma chains.
• HbF normally predominates in the first year of life.

• After that HbA predominates (96%), with HbA2 making about 2-

3%.

• Simply presence of HbS makes the disorder so called Sickle Cell

Disease.
 Types of Sickle Cell Disease
• The following are types of SCD:

• Sickle Cell Anemia

– Homozygous form, in which both hemoglobin are HbS ie. (HbS, HbS).
– Severest form.
• Sickle Cell Trait

– Heterozygous with half of hb being normal and half being sickle hb ie. (HbS, HbA).
– No symptoms unless under low oxygen tension.
• Sickle cell beta thalathemias

– Heterozygous form but with the concentration normal hb being higher than sickle hb. Mild form.
• Hemoglobin S-C disease

– There is no normal hemoglobin.

– Its form is HbS, HbC.
– Similar presentation to Sickle Cell Anemia except.
– mild and less frequent.
– 2nd most common type SCD.
– Similar mutation forms HbC except Glutamic acid is substituted by Lysine.
 Pathogenesis
• SCD is caused by a point mutation at position 6 of the beta haemoglobin gene in which a
hydrophilic glutamic acid is replaced by valine.

• The susceptible RBCs once subjected to an oxygen tension of <40mmHg for about 2-4 minutes they
become deoxygenated.

• Deoxygenated haemoglobin undergoes hydrophobic interaction with adjacent sickle haemoglobin

forming large polymer and thus RBC becomes less deformable and acquire sickle shape.

• Rigid RBCs obstruct microvasculature causing tissue hypoxia which precipitates further sickling.

• Sickle cells rapidly haemolyze and have a life span of about 10- 20 days.

• The initiation of polymerization may be incomplete and reversible if re-oxygenation occurs early in
the process.

• Repetitive exposure to alternating deoxygenated and oxygenated states can lead to membrane
distortion, oxidative damage and irreversible sickling.
Sickle Cell Trait
 Clinical Manifestation of Sickle Cell Disease
• The chief cause for admission of patients is Sickle cell crises.

• This includes the following:

– Pain Crisis
– Splenic sequestration
– Acute Chest Syndrome
– Aplastic Crisis
– Hemolytic Crisis
• The most common clinical manifestation is pain, which occurs unpredictably and is
often excruciating.

• Acute manifestations that may rapidly become life-threatening include bacterial sepsis
or severe anaemia, acute chest syndrome, and stroke.

• Other acute complications include aplastic crises and priapism.

 Factors that can Precipitate SC crises
• Infections

• Low oxygen tension

• Concomitant medical conditions (e.g., sarcoidosis, diabetes mellitus, herpes)

• Dehydration

• Acidosis

• Extreme physical exercise

• Physical or psychologic stress

• Alcohol

• Pregnancy

• Cold weather
 Vaso-oclusive Crises
• Due to obstruction of microvasculature by rigid sickle cells.

• Painful crises- can affect any part but is chiefly experienced in the abdomen, bones, joints and soft tissues.

• Starts suddenly, very severe, and it may last for several hours.

• Commonly long bones are affected, but in the 1st 18 months can involve metatarsals and metacarpals causing dactylitis
(painfull swelling hands and feet).

• Splenic sequestration

– When vasooclusion occurs in the spleen, the micro vessels blocked and blood accumulates in the spleen.
– Causes rapid enlargement and it’s a life threatening medical condition.
– Common in the first five years of life and may cause splenic infarction (autosplenism) at the end of childhood.
– Sequestration causes worsening of baseline anemia and increase risk of infection by encapsulated organism.
– This includes H. influenza, S. pneumoniae, S. typhi and N. meningitidis.

• Acute chest syndrome

– Commonly characterized by chest pain, fever, cough, tachypnea, pulmonary infiltrates, hypoxemia
– Medical emergency is commonly precipitated by chest infections in children
 Aplastic Crisis
• Worsening of baseline anemia due to infection
of parvovirus B-19.

• This is single stranded RNA virus that is

acquired by respiratory droplets and a special
philia for erythrocytes progenitor.

• Thus, switches off RBC production and causes

drastic drop of reticulocyte counts.
 Hemolytic Crisis
• Accelerated breakdown of RBC that occurs with
co-existence of G6PD deficiency.

• G6PD is a recessive X linked disorder that

results to deficiency of the enzyme required for
formation glutathione in PP pathway.

• Glutathione is required for clearing free radicals

to prevent oxidative damage.
 Chronic Manifestations
• Include anaemia, jaundice, splenomegaly,
renal disease, Cholelithiasis and delayed
growth and sexual maturation.

• Avascular necrosis of the hip and shoulder and

leg ulcers may cause chronic disability.
Clinical Spectrum of SCD
 Pediatric Problems

• All children presenting with unexplained acute

illness:
– Including acute pain in any part of the body,
anaemia, and acute neurological symptoms, loss
of vision, collapse, respiratory symptoms,
hepatosplenomegaly, jaundice, swollen limbs,
family history of SCD and sepsis should be tested
for SCD.
Diagnosis
 Clinical
• Attacks are diagnosed clinically, i.e. there is no
gold standard diagnostic test.

• Hemolysis (anemia and jaundice) is often

present, although for painful crises the
diagnosis depends essentially on how the
patient describes the pain.
 Lab Investigation
• For Screening, Diagnosis and Confirmation

• Sickling test (Hemoglobin S solubility test and sodium

metabisulfite test), not for infants. Useful after 6 month
from birth.
• Newborn Screening: HPLC fractionation (High
performance liquid Chromatography) and thin
Layer/Isoeletric focusing.
• Abnormal hemoglobin forms are detected on hemoglobin
electrophoresis a form of gel electrophoresis on which
the various types of hemoglobin move at varying speed.
• Sickle cell hemoglobin (HbSS) and Hemoglobin C with sickling (HbSC) the two most common forms
can be identified from there.

• DNA analysis.

• Other tests that may be used to help evaluate someone who is suspected of having or who is known
to have sickle cell trait or disease include:

• Complete blood Count (CBC)

• Blood Smear
• Iron Studies
• LFT
• RFT
• Electrolytes
• Chest X-ray in Acute Chest Syndrome
• Trans-Cranial Doppler Ultrasound (TCD),MRI (with or without angiography) and Neuro-psychometric
studies (NPM)
 Pharmacological Treatment
• Febrile illness

– Children with fever are screened for bacteraemia i.e. complete

blood count, reticulocyte count and blood culture taken

– Younger children (varies from center to center) are admitted for

intravenous antibiotics while older children with reassuring white
cell counts are managed at home with oral antibiotics

– Children with previous bacteraemic episodes should be admitted

• Painful (vaso-occlusive) crises

– ·Most patients with sickle cell disease have intensely painful episodes called
vasoocclusive crises.

– Painful crises are treated symptomatically with analgesics; pain management requires
opioid administration at regular intervals until the crisis has settled.

– For milder crises a subgroup of patients are managed by NSAIDs (such as diclofenac or
naproxen).

– For more severe crises most patients require inpatient management for intravenous
opioids; patient-controlled analgesia (PCA) “not applicable in our setting” devices are
commonly used in this setting.

– Diphenhydramine is effective for the itching associated with the opioid use.
• Acute chest crises

– Management is similar to vaso-occlusive crises with the addition

of antibiotics (usually a quinolone or macrolide).

– When the pulmonary infiltrates worsen or the oxygen

requirement increases, simple blood transfusion or exchange
transfusion is indicated.

– Exchange transfusion involves the exchange of a significant

portion of the patients red cell mass for normal red cells, which
decreases the percent hemoglobin S in the patient's blood.
• Hydroxyurea

– The first approved drug for the causative treatment of

sickle cell anemia.

– Hydroxyurea had previously been used as a

chemotherapy agent, and there is some concern that
long-term use may be harmful.

– It is likely that the benefits outweigh the risk.

• Splenic Sequestration Crisis

– Treatment includes early intervention and maintenance of hemodynamic stability using isotonic
fluid or blood transfusions.

– Careful blood transfusions with red blood cells are recommended to treat both the sequestration
and the resultant anemia.

– Blood transfusion aborts the red blood cell sickling in the spleen and allows release of the patient’s
blood cells that have become sequestered, often raising the hemoglobin above baseline values.

– Typically recommend only 5 mL/kg of red blood cells because the goal is to prevent hypovolemia.

– Blood transfusion that results in hemoglobin levels above 10 g/dL may put the patient at risk for
hyperviscosity syndrome because of the risk that that patient may release the blood within the
spleen.

– If there is recurrent episode Prophylactic splenectomy is the only choice for preventing future life
threating episode.
• Priapism

– The optimal treatment for acute priapism is unknown. Acutely,

supportive therapy, such as a hot shower, short aerobic exercise, or
pain medication, is commonly used by patients at home.

– Urology consultation is required to initiate this procedure, with

appropriate input from a hematologist.

– A prolonged episode lasting >4 hrs should be treated by aspiration of

blood from the corpora cavernosa followed by irrigation with dilute
epinephrine to produce immediate and sustained detumescence.
• Penicillin prophylaxis

– The most important intervention in the routine management of children

with SCD is penicillin prophylaxis to prevent pneumococcal infection,
which justifies newborn screening.

– Penicillin is given twice daily from as 2months of age.

– Children with SCD-SS are given Penicillin VK: 125mg by mouth twice daily
for those under 3yrs of age and 250mg twice daily for those 3 and older.

– An alternative to oral penicillin is an injection IM of 1.2 million units of

long acting Bicillin (Penicillin G Benzathine) every 3 weeks.
Routine Medications for SCD
 Pain Management
• Pain is the commonest acute complication in SCD.

• •
• Mild to Moderate Pain.

• •
• Use oral analgesics Paracetamol, Ibuprofen or diclofenac.

• •
• Encourage excessive oral fluids intake.

• •
• DO NOT GIVE ANALGESICS PRN But rather regularly as recommended in treatment manual.

• •
• Severe Pain.

• •
• Use Morphine PO 0.2mg – 0.5mg/Kg every 4hrs.

• •
• Give IV fluids (ref Treatment manual).
 Hydration
• Patients with SCD are at risk of dehydration due to impaired renal concentrating power and poor fluid intake.

• •
• Encourage oral fluids first, it should be used whenever possible.

• •
• Give IV fluids if the patient is unable to drink well, has severe pain, abdominal symptoms, or is not settling.

• •
• Hydrate with 150% of the normal daily fluid intake.

• •
• Use fluids recommended in pediatrics IV therapy guidelines, usually 5% Dextrose + 0.45% saline (review need for added
potassium).

• •
• Stop IV fluids when the patient is stable and pain is controlled.

• •
• Maintain a strict input/output chart for every patient.

• •
• For children, weigh them daily.
Fluid Calculations
 Prevention of Complications
• The following are recommended for prevention of acute complications:

– Early diagnosis and treatment

– Provision of routine medications such as Folic acid, Penicillin V

– Healthy diet

– Routine deworming

– Adherence to routine methods of malaria prevention

– Adequate hydration

– Avoid extremes of temperatures

– Avoid stressful environment

– Avoid demanding physical activity

– Avoid emotional stress (or learn how to better cope with it)

– Avoid tobacco and alcohol use

• Counselling

• SCA counseling has two components education and decision-making.

• Reproductive Counselling: Provide educational and health promotion counseling to all

women and men of childbearing age to reduce reproductive risk and improve pregnancy
outcomes.

• If the partner of a man or woman with SCD has unknown SCD status refer the partner
for SCD screening.

• After testing, refer couples who are at risk for having a potentially affected fetus and
neonate for genetic counseling.

• In women with SCD, regular use of contraception can decrease the health risks
associated with unintended pregnancy.
 Referral Pathway for Patients with Sickle
Cell Disease
• Give first aid and immediately refer all patients with features suggestive of severe acute
complications of SCD.

• Advise all patients to do annual screening for chronic complications of SCD at

district/regional hospital.

• Give first aid: Analgesics, Fluids, Antibiotic.

• Refer immediately : Delay may cause more harm.

• Refer all patients with features suggestive of :

• Severe anemia
• Acute chest syndrome
• Stroke
• Priapism and septicemia
Follow up Patients with Sickle Cell Disease

• Take history

• Full and thorough Examination

• Blood tests: at each visit (already said visits are yearly for
older well children

• Provide / Organise / Prescribe / Check

• Follow-up appointment to be booked

 Key Points
• Sickle cell anemia is a genetic disorder whereby red blood cells are
abnormally shaped, causing problems with the flow of blood through the
body as well as the transport of oxygen throughout the body

• Clinical presentation of Sickle cell crises includes the following:

– Vaso-occlusive crisis
– Aplastic Crisis
– Hemolytic Crisis
• Treatment includes pharmacological and non-pharmacological
interventions

• Follow-up monitoring have to be done closely by doing a complete

assessment and treatment and counselling of parents
 MANAGEMENT OF CHRONIC KIDNEY
DISEASE
• Learning Objectives
• At the end of this session participants are expected to be able to:

– Define chronic kidney disease.

– Describe risk factors, causes and classification of chronic kidney disease.

– Recognize clinical presentation and complications of chronic kidney disease.

– Provide management to patients with chronic kidney disease.

– Recognize co-management model for chronic kidney disease and patient safety.

– Implement referral pathway for patients with chronic kidney disease.

 Definition of Chronic Kidney Disease
• Abnormalities of kidney structure or function,
present for >3 months.

• Either of the following must be present for >3

months:

– Albumin Creatinine Ratio >30 mg/g.

– Markers of kidney damage (one or more*).
– GFR <60 mL/min/1.73 m2 (m squared).
 Risk Factors of Chronic Kidney Disease
• Modifiable CKD Risk Factors

– Frequent NSAIDs.
– Aminoglycosides,
– iv Contrast and Herbal use.
– Overweight and Obesity.
• Non-Modifiable

– Family history of kidney disease, diabetes, or hypertension.

– Congenital structural kidney abnormalities (Horse-shoe kidney).
– Age 40 years or older (GFR declines normally with age).
– African Ethnicity.
 Causes of Chronic Kidney Disease
• Diabetes Mellitus, Hypertension.

• Urinary bladder outlet obstruction.

• Intrarenal kidney diseases (glomerular, tubular, interstitial, or vascular).

• Kidney artery/vein stenosis.

• Chronic Heart and Liver Failure.

• Certain toxins - fuels, solvents (such as carbon tetrachloride), and lead.

• Fetal developmental abnormalities.

• Low Birth Weight, Small for Gestational Age, Prematurity.

• Autoimmune diseases (e.g systemic lupus erythematosus).

• Infections and Infestations (HIV, Hep B & C, Malaria).

• Some medications – e.g NSAIDs, iv Contrast.

• Illegal substance abuse - such as heroin or cocaine.

• Injury - a sharp blow or physical injury to the kidney.

Classification of CKD Based on GFR and
Protein in Urine
 Symptoms of CKD (non-specific)
• Blood in urine, excessively froth urine, frank pain.

• Oliguria(Reduced urine output),anuria, excessive urination at night(nocturia), pyuria

• LUTS (frequency, hesitancy, intermittency, terminal dribbling, incontinency, retention).

• Weight loss, poor appetite, nausea, vomiting.

• Oedema

• Shortness of breath

• Tiredness

• Difficulty sleeping insomnia

• Itchy skin
 Complications of Chronic Kidney Disease
• Anemia and other hematological disorders.

• Weak bones and an increased risk of bone fractures.

• Metabolic acidosis.

• Fluid retention, Electrolytes derangements especially hyperkalemia.

• Cardiovascular disorders, including pericarditis.

• Skin disorders.

• Decreased sex drive, erectile dysfunction, or reduced fertility and menstrual dysfunction.

• Pulmonary Including pleuritis,, Gastrointestinal and Neurological disorders.

• Decreased immune response.

• Pregnancy complications that carry risks for the mother and the developing fetus.

• Irreversible damage to your kidneys (end-stage kidney disease).

 Slowing CKD Progression: ACEi or ARB
• Risk/benefit should be carefully assessed in the elderly and medically fragile.

• Check labs after initiation

– If less than 25% SCr increase from baseline, continue ACEi/ARBs and monitor.
– If more than 25% SCr increase from baseline, stop ACEi/ARBs and evaluate for RAS.
• Continue until contraindication arises, no absolute eGFR cutoff.

• Better proteinuria suppression with low Na diet and diuretics.

• Avoid volume depletion.

• Avoid ACEi and ARB in combination.

• Risk of adverse events (impaired kidney function, hyperkalemia)

– Avoid combination of ACEi and ARB.

 Goals of Care in CKD: Glucose Control
• Target HbA1c ~7.0%.

• Can be extended above 7.0% with comorbidities or

limited life expectancy, and risk of hypoglycemia.

• Risk of hypoglycemia increases as kidney function

becomes impaired (Burnt-Out Diabetes Mellitus).

• Declining kidney function may necessitate changes to

diabetes medications and renally-cleared drugs.
 Modification of Other CVD Risk Factors in
CKD
• Smoking cessation

• Tolerable Moderate to Intense physical exercise (at least 150 minutes per week)

• Weight reduction to optimal targets

• Lipid lowering therapy

• Lipid-lowering therapy

– In adults >50 yrs, statin when eGFR ≥ 60 ml/min/1.73m2; statin or statin/ezetimibe

combination when eGFR < 60 ml/min/1.73m2
– In adults < 50 yrs, statin if history of known CAD, MI, DM, stroke

• Aspirin is indicated for secondary but not primary prevention

Detect and Manage CKD Complications
Anemia

– Initiate iron therapy if TSAT ≤ 30% and/or Ferritin ≤

500 ng/mL (IV iron for dialysis, Oral for non-dialysis
CKD).
– Individualize erythropoiesis stimulating agent (ESA)
therapy: Start ESA if Hb <10 g/dl, and maintain Hb
<11.5 g/dl. Ensure adequate Fe stores.
• Appropriate iron supplementation is needed for
ESA to be effective.
• CKD-Mineral and Bone Disorder (CKD-MBD):

– Treat with D3 as indicated to achieve normal

serum levels.
– 2000 IU po qd is cheaper and better absorbed
than 50,000 IU monthly dose.
– Limit phosphorus in diet (CKD stage 4/5), with
emphasis on decreasing packaged dairy products.
– May need phosphate binders.
• Metabolic acidosis

– Usually occurs later in CKD.

– Serum bicarb <22mEq/L.
– Correction of metabolic acidosis may slow CKD
progression and improve the patient’s functional
status.
• Hyperkalemia

– Reduce dietary potassium.

– Stop NSAIDs, COX-2 inhibitors, potassium-sparing
diuretics (aldactone).
– Stop or reduce beta blockers, ACEi/ARBs.
– Avoid salt substitutes that contain potassium.
– For severe/persistent hyperkalemia- give iv Calcium
Gluconate 10mg and refer for a comprehensive anti-
hyperkalemic regimen.
 Medications in CKD
• CKD patients at high risk for drug-related adverse events.

• Several classes of drugs renally eliminated.

• Consider kidney function and current eGFR (not just SCr) when prescribing meds (renally adjusted
dosing).

• Minimize pill burden as much as possible.

• Remind CKD patients to avoid NSAIDs.

• No Dual RAAS blockade.

• Any med with >30% renal clearance probably needs dose adjustment for CKD.

• No bisphosphonates for eGFR <30.

• Avoid iv contrasts for eGFR <30.

• What can primary care providers do?

– Recognize and test at-risk patients.

– Educate patients about CKD and treatment.
– Manage blood pressure and diabetes.
– Address other CVD risk factors.
– Monitor eGFR and Albumin Creatinine Ratio (encourage labs to report these
tests).
– Evaluate and manage anemia, malnutrition, CKD-MBD, and other
complications in at-risk patients.
– Refer to dietitian for nutritional guidance.
– Consider patient safety issues in CKD.
– Consult or team with a nephrologist (co-management).
– Refer patient to nephrology when appropriate.
 CKD Patient Safety Issues
• Medication errors

• Toxicity (nephrologic or other)

• Improper dosing
• Inadequate monitoring
• •
• Miscellaneous

• Multidrug-resistant infections
• Vessel preservation/dialysis access
• •
• Electrolytes

• Hyperkalemia
• Hypocalcemia, dysnatremias
• Hypoglycemia
• Hypermagnesemia
• Hyperphosphatemia
• •
• Diagnostic tests

• Iodinated contrast media: AKI

• Gadolinium-based contrast: NSF
• Sodium Phosphate bowel preparations: AKI, CKD
• CVD

• Missed diagnosis
• Improper management
• •
• Fluid management

• Hypotension
• Acute Kidney Injury (AKI)
• Congestive Heart Failure (CHF) exacerbation
 Referral Pathway for Patients with Chronic
Kidney Disease
• •Indications for Referral to Specialist Kidney Care Services for People with CKD

• Acute kidney injury or abrupt sustained fall in GFR.

• GFR <30 ml/min/1.73m2.

• Persistent albuminuria (ACR > 300 mg/g)*.

• Atypical Progression of CKD**.

• Urinary red cell casts, persistent hematuria detected.

• Hypertension refractory to treatment with 4 or more antihypertensive agents.

• Persistent abnormalities of serum potassium.

• Recurrent or extensive nephrolithiasis.

• Hereditary kidney disease.

 Key Points
• The goals of care for CKD include slow decline in kidney function, Blood pressure control.

– ≤130/80 mm Hg if there is no proteinuria.

– ≤125/75 mm Hg if there is proteinuria.
• Follow up monitoring of patients closely.

• Refer for further management.

• The goals of care for CKD include slow decline in kidney function, Blood pressure control:

– ≤130/80 mm Hg if there is no proteinuria (KDIGO 2021).

– ≤125/75 mm Hg if there is proteinuria.
• Follow up monitoring of patient closely.

• Refer for further management.