This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
Hyperkalemia
1. Management of Hyperkalemia
according to NICE Guidelines
By/Sadek Al-Rokh
Consultant Acute medicine & Endocrinology and Diabetes
(East Sussex trust UK).
MRCP (UK).
SCE Acute medicine of the royal college of physicians .
SCE Endocrine and diabetes of the royal college of
physicians.
European board in Endocrine and diabetes.
2. Grades of hyperkalemia
Mild Hyperkalaemia
5.5 – 5.9 mmol/L If eGFR has not increased
>10% or no acute increase in K
can repeat in 1-2 weeks.
Review medications & diet for
causes.
Moderate Hyperkalaemia
6.0- 6.4 mmol/L Recheck ASAP.
If ECG changes admit.
Stop medications that may
elevate K.
Severe Hyperkalaemia
≥6.5 mmol/L or if ECG
changes present
Urgent repeat: Admit
3. Causes of Hyperkalemia
Decreased potassium excretion
Drug induced:
Potassium sparing diuretics (Spironolactone, Amiloride, co-amilofruse)
ACE inhibitor, ARBS, NSAIDs , Beta blockers, Digoxin Excess, Cyclosporine, tacrolimus,
Heparin)
Renal failure (Acute or chronic).
Addison disease.
Type IV renal tubular acidosis.
Shift of potassium into extracellular space
Metabolic acidosis (i.e. DKA).
Rhabdomyolysis , Tumor lysis syndrome ,
Hemolysis.
4. Causes of Hyperkalemia
Increased potassium intake
High-potassium, low-sodium diets.
Ingestion of potassium supplement.
Entral feeding (Glucerna , Ensure).
PRBC transfusion (risk peaks at 2-3 weeks of cell storage)
Pseudohyperkalemia(Spurious hyperkalemia)
(Potassium high in blood sample but not in patient):
Traumatic venipuncture.
Delay in reaching laboratory.
Contamination with EDTA (FBC) in tube.
Haemolysis during venipuncture or excess cuff time.
Thrombocytosis –Leukocytosis.
6. Signs and Symptoms of hyperkalemia
Neuromuscular symptoms (Muscle weakness and paresthesia).
Hypotension.
Syncope (due to arrhythmia).
ECG changes (Bradycardi and arrthmia as prescribed below ) :
7. Investigations & Monitoring :
Repeating serum potassium urgently is necessary to exclude spurious
hyperkalaemia, especially if hyperkalaemia is unexpected or an isolated finding
and there are no ECG changes in the patient.
Serum creatinine&Urea and Electrolytes for possible AKI or CKD.
Venous blood gas sample. Serum potassium levels may be assessed on an arterial
or venous blood sample using a point of care blood-gas analyser in emergencies
whilst awaiting a formal laboratory result.
Monitor U &Es and venous bicarbonate – for possible Acidosis (e.g. renal failure,
renal tubular acidosis, hypocortisolism).
Continue to monitor serum potassium and response to treatment or possible
potassium rebound by rechecking U & Es:
1 hour after treatment commenced
At least every 6 hours until potassium within normal range
Conduct a 12-lead ECG – this is mandatory for all patients with raised serum
potassium levels prior to treatment of hyperkalaemia. Note the ECG may not
demonstrate changes even in the presence of severe hyperkalaemia.
Monitor blood glucose levels to exclude hypoglycaemia prior to commencing
treatment. If hypoglycaemia is present treat according to hospital hypoglycemia
management pathway.
8. Treatment of Severe Hyperkalemia :
If serum potassium is > 6.5 mmol/L or any
hyperkalaemia is accompanied by ECG changes
or symptoms then seek advice and give urgent
treatment as below :
1-ECG monitoring :
A 12-lead ECG is mandatory in patients with severe hyperkalaemia.
The ECG does not always demonstrate changes even in the presence of
severe hyperkalaemia so a normal ECG does not exclude the need for
urgent treatment.
Patients with a serum potassium > 6.5 mmol/L or features of
hyperkalaemia on a 12- lead ECG should receive continuous
monitoring with a minimum of a 3-lead ECG.
Patients with a serum potassium of 6.1 – 6.4 mmol/L who are clinically
unwell or where a rapid rise of serum potassium is anticipated should
also receive continuous monitoring via a 3-lead ECG (preferably in a
high care setting).
9. Treatment of Severe Hyperkalemia
2-Protect cardiac membrane :
Give 10mL of calcium gluconate 10% intravenously via slow IV bolus into a large peripheral
vein over 10 minutes.
If central venous access is available 10mL of calcium chloride 10% administered slowly via
a central line over 3-5 minutes is first-line treatment option due to its greater efficacy. Note:
this injection must not be administered peripherally due to the potential for venous irritation
and tissue necrosis from extravasation.
These treatments do not lower serum potassium but if ECG changes are present there
should be an improvement seen in the ECG within 1-3 minutes.
A normal ECG does not negate the need for calcium gluconate or calcium chloride 10%
injection.
A further 10mL of calcium gluconate 10% or calcium chloride 10% (central venous access
only) should be administered IV every 10 minutes if no improvement is seen initially until the
ECG normalises, up to a total of 50mL can be administered.
The effect of this treatment is transient and lasts 30 minutes.
If patients are on digoxin 10mL of calcium gluconate, 10% injection should be mixed with
100mL of glucose 5% and administered slowly intravenously over 20 minutes. (Rapid
calcium administration can precipitate myocardial digoxin toxicity).
Administration of calcium gluconate 10% or calcium chloride 10% injection does not lower
serum potassium therefore other interventions are urgently required.
10. Treatment of Severe Hyperkalemia
3-Shift potassium from blood into the cells :
Administer Insulin/glucose infusion.
Check blood glucose levels first prior to infusing insulin and correct hypoglycaemia
in the patient if presentز
Add 10 units of soluble insulin (Actrapid® ) to 50mL of glucose 50%. Infuse over 15
minutes intravenously via an infusion pump. This can be administered peripherally,
ideally into a large vein.
The onset of hypokalaemic action occurs within 15 minutes after the start of the
infusion & lasts around 60 minutes.
The administration of insulin/glucose infusion can be repeated. Administer up to
three times to lower serum potassium levels.
Monitor for hypoglycemia and check blood glucose levels 30 minutes after
commencing infusion, followed by hourly checks up to 6 hours after the infusion has
finished as delayed hypoglycaemia can occur.
If hypoglycaemia does occur glucose tablets/gel should be used in preference to
orange/fruit juice due to its high potassium content.
Check Urea & electrolytes 30 minutes after each insulin/glucose infusion. If there is a
good response U & Es can be checked 1-2 hours later after the last infusion.
11. Treatment of Severe Hyperkalemia
4-Administer salbutamol via nebulisation
Give salbutamol 10mg – 20mg via nebulisation.
Its effects are seen within 15-30 minutes lasting up to 2 hours.
Patients with ischemic heart disease should receive the lower dose of
10mg.
Avoid in patients with significant tachycardia (heart-rate > 120bpm).
Salbutamol should never be used as monotherapy for the treatment of
severe hyperkalaemia as some patients may not respond to this
treatment. Treatment using a) and b) in patients has additive effects in
lowering serum potassium levels so should always be prescribed
together for best results.
12. Treatment of Severe Hyperkalemia
5-Stop further potassium accumulation :
Review & stop all potentially offending drugs or infusions on drug chart.
Beta-blockers and digoxin should also be reviewed (and witheld temporarily if it safe
to do so) as they reduce the effectiveness of salbutamol nebulizer & insulin-glucose
infusion.
Place the patient on a low potassium diet.
Correct underlying cause of hyperkalaemia (i.e. acute kidney injury, sepsis)
6- Haemodialysis :
If serum potassium levels remain high in a patient (>7 mmol/L) despite the
administration of first-line measures above or ECG changes/symptoms persist the renal
team should be contacted to arrange urgent dialysis as appropriate.
Early referral to the renal team/ITU for advice and management is vital to allow time to
organize this management plan.
Hemodialysis is the most effective and definitive method in treating hyperkalaemia by
actually removing potassium from the body but it is invasive.
13. Treatment of moderate Hyperkalemia :
If serum potassium is 6.0 to 6.4 mmol/L AND ECG
changes and symptoms are absent then give the
following treatment for patients with non-severe
hyperkalaemia:
A 12-lead ECG – is mandatory for all patients with serum potassium levels >6.0
mmol/L prior to treatment of hyperkalaemia.
Review and stop all potentially offending drugs or infusions on drug chart.
Beta-blockers and digoxin should also be reviewed (and witheld temporarily if it
safe to do so) as they reduce the effectiveness of salbutamol nebules & insulin-
glucose infusion.
Place the patient on a low potassium diet.
Correct underlying cause (i.e. acute kidney injury, sepsis).
14. Treatment of moderate Hyperkalemia :
Administer Insulin/glucose infusion (Discussed before).
Administer salbutamol via nebulization (Discussed before).
Remove potassium from the gut – cation-exchange resins (Calcium polystyrene
sulphonate) resin (Calcium Resonium® ) 15 grams orally 3-4 times daily.
The powder should be given in a small amount of water.
The onset of action is slow (>2 hours) and therefore cation-exchange resins do not
have a role in the emergency treatment of patients with severe hyperkalaemia.
Prescribe with regular lactulose solution 15 mL orally twice daily will help increase gut
losses of potassium and prevent constipation.
If the oral route is unavailable, calcium resonium 30 grams can be administered
rectally as an enema. The solution must be retained for 9 hours followed by irrigation
of the colon to remove resin and prevent faecal impaction.
Administration of Calcium Resonium® orally or rectally is contraindicated in: - Patients
with obstructive bowel disease, - Conditions associated with hypercalcaemia, -
Patients with serum potassium levels >5.
15. Treatment of mild Hyperkalaemia :
If serum potassium is < 6.0 mmol/L AND ECG changes
and symptoms are absent then give the following
treatment for patients:
Temporarily stop all potentially offending drugs or infusions on drug
chart.
Put the patient on a low potassium diet.
Correct underlying cause of hyperkalemia (i.e. acute kidney injury,
sepsis).
Consider removal of potassium from the gut – cation-exchange
resins (Discussed before).
16. Post treatment checklist :
Following management of hyperkalemia according to the above
guidelines:
Recheck serum potassium levels daily during the patient’s
admission and periodically thereafter.
Review any medication(s) stopped during an acute episode of
hyperkalemia and restart if necessary with close monitoring. For
example it may be necessary to restart a patient’s ACE-inhibitor
which could be reintroduced at a lower dose after an isolated case
of hyperkalemia secondary to AKI. Digoxin may need to be
recommenced and a lower dose could be recommenced with
close serum monitoring in the patient. Contact Pharmacy for
advice. Provide the patient with dietary advice on maintaining low
potassium intake if needed (i.e. patient’s with CRF).
17. Treatment in Cardiac arrest due to hyperkalemia:
Follow the standard advanced life support (ALS) algorithm including basic life support
(chest compressions & ventilation). The following treatment steps are recommended
by the Resuscitation Council UK:
In patients presumed to be in cardiac arrest secondary to hyperkalaemia use a blood gas
analyser to rapidly confirm a diagnosis of hyperkalaemia.
Administer treatment to protect the cardiac membrane first followed by the administration of
treatments to shift potassium from the blood to inside the cells.
Administer 10 mL of calcium chloride 10% by rapid Intravenous bolus via peripheral or central or
intraosseous (IO) access. In cardiac arrest only calcium chloride 10% is permitted to be
administered via a rapid intravenous bolus peripherally.
Administer sodium Bicarbonate 50mmol by rapid intravenous bolus via peripheral or central or IO
access.
Do not give calcium solutions and sodium bicarbonate solutions simultaneously by the same
route.
Administer insulin/glucose infusion: Add 10units of soluble insulin (Actrapid®) to 50mL of glucose
50% and administer by rapid intravenous injection via peripheral or central or IO access. Rapid
administration of insulin/glucose infusion for the treatment of hyperkalaemia is only permitted in
patients who have suffered a cardiac arrest.
The treatment steps can be repeated according to the clinical condition of the patient and the
results of a repeat blood gas analysis.
Consider hemodialysis in patients who have suffered a cardiac arrest induced by hyperkalaemia
which is resistant to medical treatment. Contact renal/ITU team urgently for advice.
18. Treatment of hyperkalemia due to digoxin toxicity
Digoxin toxicity in a patient (especially in renal failure) can
lead to hyperkalaemia & arrhythmias. Serum digoxin levels
should be checked and monitored in patients with
suspected digoxin toxicity and the offending drug
discontinued.
The administration of digoxin-specific antibody fragments
(Digifab®) may represent the preferred approach of
treatment of a patient. Consult with senior colleagues and
seek advice from Pharmacy.
19. Use of Sodium Bicarbonate in treatment of
hyperkalemia
An infusion of sodium bicarbonate is usually not recommended.
Whilst this has been a traditional treatment option for
hyperkalaemia, studies have shown there are potential risks in
giving a sodium bicarbonate infusion in terms of volume and sodium
overload and tetany in patients with chronic renal failure and co-
existing hypocalcaemia.
The risks are thought to outweigh potential benefit in most cases.
However, in the presence of significant metabolic acidosis
(Bicarbonate < 15 mmol/L) it may be appropriate to administer
sodium bicarbonate.
Administration of Sodium Bicarbonate 1.26%. Advice from the renal
team must always be sought prior to its use.