This patient presented with acute onset quadriparesis due to severe hyperkalemia. Laboratory investigations revealed high serum potassium of 8.7 mEq/L, metabolic acidosis, renal dysfunction, and glucosuria. The hyperkalemia was likely due to a combination of factors - decreased renal excretion due to recent initiation of ACE inhibitors and spironolactone for hypertension, worsening of renal function due to NSAID use and UTI, and potassium shift into extracellular space due to severe hyperglycemia and acidosis. Immediate treatment focused on reducing potassium levels while the underlying causes were addressed.
2. Fluid and electrolyte disturbances
⢠Most common clinical problems encountered in ICU.
⢠Increased morbidity and mortality among critically ill
⢠Disturbances of monovalent ions (Na, K, Cl) and divalent
ions (Ca, PO4 and Mg)
⢠K, Mg and PO4 are mostly intracellular cations. Cl exists
in the extracellular space, at electrochemical equilibrium
with Na.
Electrolyte blood press
V8 (2);dec 2010
3. Fluid and electrolyte disturbances
⢠An alteration in this ratio: significant effects on acid base
balance
⢠Disorders like trauma, sepsis, brain damage, and heart
failure cause disturbances in fluid and electrolyte
homeostasis.
⢠Mechanisms:
â reduced perfusion to the kidney (hypovolemia or
hypotension)
â
â activation of hormonal systems such as RAAS and AVP
â Renal tubular damage.
4. Fluid and electrolyte disturbances
⢠Most important: inappropriate fluids
⢠Formulae to guide the therapy:
â All formulae regard the patient as a closed system
â none takes into account ongoing fluid losses that are
highly variable between patients
â Therapy must be closely monitored with serial serum
and urine electrolyte measurements.
Semin Dial. 2006 Nov-Dec;19(6):496-501.
8. Hyponatremia- Define it
⢠Relative water excess
Sr Na < 136 Meq/ L
â Low water and lower sodium content in the body
Hypovolemic hyponatremia
Extracellular fluid volume contraction (true volume depletion)
Syndrome of appropriate ADH secretion
10. Hyponatremia- Define it
â Normal or excess Na, and still higher H2O content
CHF, Nephrotic syndrome, cirrhosis of Liver
Non osmotic release of ADH
âEffectiveâ circulating volume contraction
12. Donât forget ADHâŚ..
⢠Water surplus/ excess aloneâŚ.
â Excess free water (electrolyte free water) ingestion alone
â will result in large quantity of maximally diluted urine
â So only water surplus â cannot cause/ sustain
hyponatremia
â ADH â almost always present
â What we want to know is why is the ADH present?
13. Symptoms and signs
of hyponatremia
⢠None
⢠Headache
⢠Lethargy
⢠Dizziness and ataxia
⢠Mild confusion
⢠Psychosis
⢠Seizures
⢠Coma
23. Endocrine factors- remember
⢠Hypothyroidism
â commonest electrolyte
derangement in
hypothyroid
â Hyponatremia : 45% of
hypothyroid patients
â Easily identified and
correctable
⢠Addisons:
⢠hypersecretion of
ADH
⢠Hyponatremia
corrected by cortisol
and volume repletion
⢠shuts off ADH release.
24. Case 1
⢠66 yrs old lady, HT since 5yrs
⢠1 month ago: BP- 160/94, thiazide added to amlodep
⢠Progressive lethargy, fatigue, only taking liquids.
decreased urine output.
⢠Confused since 1 day- GTCs 1 hr ago
⢠Hospitalized: 60 kg (previously recorded)
â HR- 100, BP 130/70, low JVP, post ictal state.
â Appeared volume depleted
25. Case 1
⢠Treatment:
â Catheterized- 200 ml immediately removed,
blood tests sent, IV access, Ryles tube
â FPBS- 106, IV NS 1000 ml over 1/2 hr
â Noted urobag to be full- staff assumed
retention, everyone happy.
26. We got the blood testsâŚ..and I was worried
Parameters Blood urine
Na 125 8
K 3 10
Cl 62 12
Total protein 8.4
Hb / Hematocrit 17 gm/ 51%
HCO3 30
Urea 55
Creatinine 1.6
Ca 9.5
27. Case 1
more worried when diuresis occurred
and Na changed rapidly
Repeat Sr Na, exactly 2 hours later
135 Meq/L
Urine output was 2L in 2 hours
28. Case 1
⢠Why did this happen?
⢠Risks?
⢠What went wrong?
⢠What do we do next?
29. Case 1- why did this happen
⢠Lets calculate what went in and how much should have the
Sr Na changed.
â TBW= 30 L (50% of weight in females)
â Given 150 Meq/ L of 0.9 % NS (ie 1 L of H2O + 150 Na)
â Na deficit (Na to be replaced to achieve a particular Sr Na
Level) = TBW (desired Na- actual Na)
â 150 Meq/L = 31 L (x- 125 Meq/L).
â âXâ is what the Na should be, if we replace 1 L of 0.9% NS
â X = 5 Meq/ L
30. Why did this happen ?
⢠ADH shut off- volume
replacement
⢠Free water diuresis-
â Electrolyte free water is
excreted
â So if H2O is removed from
body, Na concentration
rapidly increases
31. Risks
⢠Osmotic demyelination
syndrome (ODS or CPM)
â Under estimated incidence
â Critically ill ICU patients,
difficult to diagnose
â Brain shrinks with rapid
correction of Na
â No treatment, prevention
pons
Non pontine areas
32. What went wrong?
⢠Classify hyponatremia
â Acute Vs Chronic is the only useful one for treatment
â Most chronics have an acute component
â In our case, even before we classified it, we corrected it
inadvertently
â Lady definitely had and acute component, excessive water
drinkingâŚ.
⢠Why did the Na correct so rapidly even with 150 Meq/L
of Na?
33. What went wrong?
Why did the Na correct so rapidly?
Thinking beyond the algorithm for Na correction
⢠1 L of 0.9 % NS (150 Meq/L of Na)- the Sr Na
should â by 5 Meq/ L
⢠Why did it go up so rapidly?
The concept of tonicity balance
What goes in and what comes out?
34. Tonicity balance
Input
1 L NS
i.e. 1 L of H2O
+ 150 Meq (Mmols)
Of Na
Body compartment
Na and water Content
Output
2 L urine
U Na + K = 40
i.e. 2 L of water
And 40 mol Na +K
30 L TBW in 60kg female
30 L of water
3750 Mmols Na
35. Tonicity balance- new body content
of Na and water
Body compartment
New Na and water Content
30 L TBW in 60kg female
Water= 30+1-2=
29L
Na: 3750+ 150-40
3910
Sr Na = 3910/ 29
134.8
And that was
Our Sr Na after
2 hours
36. Why GTCs at Na of 125??
⢠1st
- we check Venous Na, not arterial.
â Brain sees arterial Na, not venous.
â Arterial Na 3-5 Meq/L lower than venous Na
⢠2nd
and more important-
â Post GTCs: seizures increase Sr Na!!!
â During seizures: water shifts in muscle cell- Sr Na can
rise by 10 to 15 Meq/L after seizures
37. Donât forget the water in GI tract..
⢠Most cases of acute on chronic hyponatremia,
occurring at home- solute free water intake/
fruit juices etc â water source
⢠Insert RT in hyponatremic convulsion-
remove water in stomach if its there
38. Remember about K correctionâŚ.
⢠Most body K â intracellular
⢠K replaced for correction of hypokalemia:
â Enters the cells, intracellular Na comes out
â So giving 80 Meq/L of K is equivalent to giving
Na
â K replacement is equivalent to giving Na
39. Back to our Case
⢠Lower the Na: 1 L of 5D = will decrease Na by 5Meq/L
â 3910/30= 130
⢠Stop further diuresis of free water: DDAVD
(desmopressin)
â Ideally IV 2 to 10ug, till urine output < 100 ml/hr
â Used 20 ug intranasal- decreased diuresis
⢠6 hrly monitoring of Sr and urine electrolytes
⢠Replace what comes out (urine)- volume + electrolytes
40. Replace what comes out (urine)
⢠Urine 100 ml/ hr, Urinary Na + K = 70
â Give half NS with Na content of 75 meq
â This will prevent further rise
⢠Free water restriction to < 1 L/ day
41. Summary of guidelines for therapy
⢠Classify acute Vs Chronic- history, change in
medications
⢠Assess volume status
â Most reliable hematocrit and total Sr. proteins
â Urine electrolytes (UNa < 10)
â Hemodynamic and clinical: least reliable
⢠Therapeutic considerations in acute hyponatremia and
diagnostic considerations in chronic hyponatremia
42. Summary of guidelines for therapy
⢠Acute component of Chronic:
â Raise Na by < 5 Meq/L, use 3% NS
â Later fluid restriction and find the cause
⢠Ask 2 questions in the patient with low Na
â Why is the ADH present?
â Will the release of ADH cease and cause rapid
water diuresis?
43. Specific to ICUs
⢠Symptoms may not be apparent in ICUs
â ventilated and sedated patients in the ICU
â worsening of cerebral edema
â catastrophic consequences such as brainstem
herniation and respiratory arrest.
44. Copyright Š2006 American College of Cardiology Foundation. Restrictions may apply.
deGoma, E. M. et al. J Am Coll Cardiol 2006;48:2397-2409
Vasopressin (AVP) stimulates synthesis of aquaporin-2 (AQP) water channel proteins and
their transport to the apical surface of collecting duct principal cells
TOLVAPTAN
NOT in hypovolemic
Hyponatremia
47. K physiology
⢠Total body K stores are approximately 3000 meq
⢠K: primarily intracellular cation {98 % of body K}
⢠Ratio of the K concentrations in the cells and outside:
major determinant of the resting membrane potential
across the cell membrane
⢠Generation of the action potential: essential for normal
neural and muscle function
⢠K abnormalities: Muscle weakness and arrythmia
48. Regulation of urinary potassium excretion
Connecting segment & Cortical duct
Na comes here
Lumen
Negative
ROMK
Electrical gradient
For K secretion
Na-K ATPase
Electrical and
chemical
gradient for Na
reasbsorption
49. Regulation of urinary potassium excretion
Stimulation of K secretion by principal cells
⢠An increase in plasma potassium
concentration and/or potassium intake
⢠An increase in aldosterone secretion
⢠Enhanced delivery of sodium and water to
the distal potassium secretory site
50. An increase in plasma potassium
concentration and/or potassium intake
51. An increase in aldosterone secretion
Hyperkalemia
Renin angiotensin
Aldosterone system
(RAAS)
Na channel
Aldosterone deficiency,
blockade
52. Enhanced delivery of sodium and water
to the distal potassium secretory site
We need Na and
Water here.
No distal Na (decresed GFR),
No K secretion
e.g Renal failure
Increased distal flow,
Increased Na delivary,
Increased K secretion
Eg diuretics
53. Distribution of potassium between the
cells and the extracellular fluid
98 % K intracellular
Maintained by this
pump
Pump block
eg digitalis toxicity
Beta blockers
Pump stimulation
Insulin, beta2 stimulation
56. Hyperkalemia
⢠Increased intake: K adaptation, rapid
⢠Shift: intracellular to extracellular, alone again not
enough to sustain hyper K.
⢠Decrease excretion: almost always present
â Aldosterone
â Decreased distal delivery of Na/ water
â Renal dysfunction
57. Case 1
⢠52/ male, DM and HT- 15 yrs
⢠Uncontrolled HT, Edema 3+
⢠Recent change in medications
⢠Adm: rapid onset quadriparesis over last 24
hours
58. Case1: examination
⢠ECG: HR of 30, broad QRS, CHB like pattern
⢠Rest vitals stable
⢠Higher functions normal
⢠Quadriparesis (grade 2 power, absent reflexes)
59. Case 1: Labs
⢠Na 129
⢠K 8.7
⢠Cl 96
⢠HCO3 16
⢠AG 17
⢠Creat 4.4
⢠Glucose 600
⢠CBC leucocytosis
⢠Urine
⢠Sugar- 4+
⢠Ketones- nil
⢠Plenty pus cells
62. Case analysis
⢠Decreased renal excretion (almost always)
⢠Was started on ramipril (ACEI) for HT
â RAAS blockade (decreased aldosterone)
Decreased GFR
so decreased distal delivery of Na and water,
no Na reabsorption, no electronegative potential in lumen
No secretion of K
64. Case analysis
⢠The patient was also
started on
spironolactone which
blocked aldosterone
action
⢠NSAIDS for fever
â Deceased GFR
â Renal failure
65. More mechanisms
⢠K loading increases ROMK expression and insertion into
CCD luminal membrane
⢠? May be gut signal to kidney to change ROMK
⢠Another K channel in CCD
â High capacity K channels (big K or Maxi K)
â Activated of high flow (water and Na delivery)
â Activated by K depletion
â Aldosterone independent action
66. Another K channel: intercalated cells
⢠H-K exchanger in IC
cells of CCD
⢠Activated in K depletion
⢠Absorbs K+ and
secretion of H+
67. Evaluation of hyperkalemia
⢠Exclude Pseudohyperkalemia
â potassium movement out of the cells during or after
the blood collection
â Torniquet
â Thrombocytosis, high WBC counts (leukemias)
68. Assessing K excretion
⢠Kidneys can vary K excretion from < 5 Meq/L to 400
Meq/L, with decreased or increased intake
⢠Urine K/ Creatinine ratio
â < 15 mmol/gm in K depletion
â >200 mmol/gm in hyperkalemia
â
69. Case 1
⢠Urine Na- 120 Meq/L
⢠Urine K- 15 Meq/L
⢠SO distal delivery of Na is adequate
⢠Severely impaired K excretion
⢠Aldosterone deficiency: hyporeninemic
hypoaldosteronism in DM
⢠Drugs blocking aldosterone production and action
⢠Decreased GFR
70. Case 1
⢠NSAIDS: worsening of RFT (GFR)
⢠PG synthesis inhibited
â PG inhibit renin âreduce aldosterone
⢠So in this patients, almost all things to increase
his K has been done
â ACEI, aldosterone blockade
â NSAIDS
71. Treatment of severe hyperkalemia
⢠Calcium: if hypocalcemia or ECG changes
⢠Shift inside the cells:
â Insulin alone (hyperglycemia) or with 25 %
Dextrose
â B2 agonist
â Bicarbonate if acidosis
72. Treatment
⢠Excretion
â Saline, especially if depleted
â Thiazide and loop diuretic
â K binding resins, small effect, increasing GI
excretion, given with lactulose
⢠Dialysis- the most rapid and effective means in the
presence of renal dysfuction and fluid overload
73. Case 1
⢠We started the patient on dialysis, normal
sinus rhythem in 45 minutes
⢠Stopped implicated drugs, treated UTI
⢠Baseline creatinine of 2 mg % on follow up.
⢠K normal
74. The message..
⢠Increase intake- not sufficient
⢠Hyperkalemia is always a kidney problem
⢠Consider shift
⢠Drug history very important
⢠Assess excretion
â Urine electrolytes- distal Na delivery
â Aldosterone deficiency/ block
â Urine K/ Creatinine is important
77. In ICUsâŚ.
⢠Upto 20% of patients
⢠Symptoms: mainly neuromuscular
⢠Risks:
â Respiratory muscle weakness, difficult to wean
â Life threatening cardiac arrthymias
â Paralytic ileus, risk of transmigration, nutrition
78. hypokalemia
⢠Low intake: possible, if prolonged, critically ill
â Kidneys can decrease excretion < 20 Meq/ day
â Low intake alone, not be sufficient unless severe
⢠Shift very important in this settings, drugs
⢠Excretion: diuretics
â Drugs like amphoterecin B
â Non absorbable anions- penicillins
79. Case 1
⢠62/F, diabetic- 10 yrs, HT
⢠Admitted with fever, cough, SOB: 8 days
⢠Pneumonia
⢠Anorexia, severe nausea
⢠Meds- insulin, amlodepine, thiazides
⢠HR- 130, BP- 766/50, volume depleted
81. Case 1
⢠CAP: levofloxacin, pipericillin- Tazobactum
⢠IV insulin 20 units bolus, Insulin drip
⢠IV NS 1 L bolus, another 1 L after an hour
⢠BP 80/50
⢠Dopamine drip
⢠6 am, inablility to move limbs
⢠Intubated because of hypoventilation, hypoxia
82. Case 1
⢠Na- 134, K- 1.8, Cl-102
⢠Urine output- 1200 ml
⢠Urine K- 20 Meq/L, Na - 12
Where did the K go?
83. Case analysis
⢠Intake- poor, nausea
â Likely lower body content: thiazides
â Hyperglycemia (sepsis)- osmotic diuresis
⢠Initial K normal: shift out of cells
â Hyperglycemia
â Insulin deficiency
87. Case analysis: Renal excretion
⢠Distal delivery of Na and K: NS infusion
⢠Diuretics: increase distal delivery of Na and
Water
⢠Hyperglycemia: Osmotic diuresis
91. Renal excretion: non-reabsorbable anions
⢠Like β-hydroxybutyrate in DKA,
â penicillin derivative in high dose penicillin therapy
⢠Accompanying Na ions, increased distal delivery, more Na
reabsorption, more lumen negative
⢠Final pathway here is increased distal Na delivery
93. Extra renal loses
⢠Loss of gastric secretions (vomiting, aspiration)
â Little K in gastric juice
â Loss of H+ met alkalosis increased HCO3 + Na
â Na exchanged with K
⢠Diarrhea: K content in intestinal juices (30- 50 meq)
â˘
94. Case analysis
⢠Decreased intake- yes, low stores (thiazides)
⢠Shift: definitely
â Insulin
â Beta stimulation
⢠Excretion: NO. Urine Na and K,
appropriately low
Disturbances in fluid and electrolytes are among the most common clinical problems encountered in the intensive care unit (ICU). Recent studies have reported that fluid and electrolyte imbalances are associated with increased morbidity and mortality among critically ill patients. The dyselectrolytemias include disturbances of monovalent ions like Na, K and Cl and divalent ions ions like Ca, P , Mg. Potassium, magnesium and phosphate are mostly intracellular cations, and chloride exists in the extracellular space, at electrochemical equilibrium with sodium. An alteration in this ratio can have significant effects on acid base balance â chloride depletion causes alkalosis, chloride excess causes acidosis.
Potential mechanisms for such electrolyte disturbances include decreased renal perfusion, hormonal disturbances like RAAS and AVP. ATN. Most important is inappropriate admisnistration of fluid and electrolyte.
Eg: in a case of hypovolemic hyponatremia, the urinary losese are usually very low. As against this, in a case of Hyponatremia due to SIADH, the urine losses almost all Na that has been replaced. So in both situations, at the same level of hyponatremia, the amount of Na that needs to be replaced varies.
This is not a single topic. Actually itâs a vast, and appears very complicated- actually it is very complicated. My teacher at university of toronto, Dr Kamel Kamel, who has a 100 papers on this topic, a world authority always said âNo hyponatremia is enough hyponatremiaâ. He meant it in the matter of teaching.
Iatrogenic is without considering the patients physiology, inappropriate kind of IV fluids are administered. The fact is there is no fixed protocol for prescribing a particular type of fluid in a particular type of patient.
You have to consider the clinical situation, and factors that can release ADH (anti diuretic hormone) in that situation.
Secondly, calculate the expected loses, and replace accordingly, there is no need of additional fluids unless hemodynamically stable. Why do we need a fixed prescription of 2 RLs, 2 DNS, and one 5% D as a routine postoperatively?. In addition to the losses, only 500 ml of fluids are adequate to excreate all the solutes in one day.
In sodium and water physiology termsâŚ. It is defined as relative water excess, In biochemical terms a sr Na &lt; 136 Meq/ L
It can occur in 2 circumstances: 1. Low total body content of water, and low sodium- renal or non renal loses, Hypovolemic hyponatremia, the syndrome of appropriate ADH secretion
2. Na retention, and still higher water content
Effective circulating volume contraction e.g. CHF- fluid in venous compartment and arterial compartment volume is low, very poor Ejection fraction- so behaves as if you have hypovolemia.
Nephrotic syndrome and cirrhosis- ECF is expanded, but the fluid is interstitial or third spaced
High extracellular fluid volume- still water in excess.
So in both the situations, we know that there is relative water excess.
Ingestion- IV or oral.
Maximally dilute- the urine osmolality in a young healthy adult can vary from 70 mosm/L to 1400 mosm/L
You need slight concentration with this chart, not difficult. Will make rest of the understanding very easy
In individuals, the Sr Osmolality is kept in a very narrow range. Every one has a osmotic set point. Even if there is a slight change in the osmolality, ADH increases or decreases to bring back the osmolality to that point.
So ADH is very sensitive even to a very slight change in osmolality.
As you can see, ADH significantly rises only after more than 10% of the blood volume is lost&gt;
Otherwise a healthy lady
She was immediately catherterised as she was confused, appeared volume depleted so was treated with IV fluids. Actually she was not hemodyanmically unstable.
In our unit and may be all nephro units, everyone looks at they urobag first then at the patient (before checking whether he is breathing or not).
With this patient, we had previous routine evaluation available which were done around 6 weeks ago, and there was not intercurrent illness.
So definitely hyponatremia, hypokalemia
Na deficit to be replaced is equal to Total body water (which would be 50% of the body weight in females) multiplied by the expected change in sodium. We have replace 150 Meq/L of Na. 1L NS contains 154 Meq/L of Na.
ADH secretion starts when &gt; 10% of the blood volume is lost â i.e. significant volume depletion. When that small volume is replaced, ADH shuts off- No more water channels in the MCD, so free water diuresis
1. Previously called Central pontine myelinosis, now ODS. As is can also occur in other non pontine areas.
2. Incidence is grossly underestimated, as it occurs in critically ill ICU patients with multiple complications and ventilated. So it is difficult to judge.
3. MRI changes appear approximately 3 weeks after the insult, so we need to rule out other causes of diffuse encephalopathy. So initially itâs a diagnosis of exclusion.
No treatment available and so only thing we can do is prevention.
There have been multiple classification for hyponatremia- hypovolemic, normovolemic, hypervolemic, OR appropriate ADH vs inappropriate ADH. Almost all these classifications are imperfect
The only useful classification that is useful for treatment is Acute Vs chronic
We have previously calculated that the Na should correct only by 5 Meq/ L, which would have been very appropriate in the present clinical scenario.
Remember Sr concentration of Na = total body content of Na / total body water.
Where did this 3750 mmol (meq)/ L of Na come from?- 30 L multiplied by Sr Na conc (125)
Remember Sr concentration of Na = total body content of Na / total body water.
Where did this 3750 mmol (meq)/ L of Na come from?- 30 L multiplied by Sr Na conc (125)
We would definitely get a history that the patient has been drinking water for the past few days. At least we will remove the extra water that has been ingested in last few hours.
6 hrly- there is no alternative to close monitoring of electrolytes, atleast for the first 48 hours
Replace what comes out-
Luckly our patinet did not develop neurological deterioration.
Use 3% NS to raise the Na by &lt; 5 Meq/ L
Frequent monitoring is the Key
These are Aquaporin type 2 receptor blockers, and thus prevent action of vasopressin. Improve free water clearance, esp in cases where cause of high ADH cannot be corrected&gt;
Resting membrane potential for required in all neuromuscular functions
An increase in plasma K stimulates aldosterone, which increases the activity of basolateral Na-K ATPase, thus creating a base of reabsorbtion of Na and then K secretion
So aldosterone excess will lead to hypokalemia and deficiency or blockade will lead to hyperkalemia
Now once we understand the physiology, it is very easy to evaluate a patient of hyperkalemia
So severe hyperglycemia, as occuring in DKA/ HONKS can cause shift of K out of cells and cause hyperkalemia, even though, there is deficiency of total body potassium. So when we correct these conditions with insulin, the K shifts back to cells and actually cause significant hypokalemia, and replacement is necessary
Vigorous exercise and rapid breakdown of cells (like rhabdomyolysis after crush injury, tumor lysis after chemotherapy for hematological malignancies etc) can cause transient hyperkalemia. This becomes clinically significant when its associated with renal dysfunction
Insulin stimulatess
Increased intake of K alone is not enough to cause hyperkalemia. Our kidneys can adapt to increased intake from 100 to as high as 400 Meq/day. Can occur independent of aldosterone- increased density of apical ROMK and basolateral Na-K ATPase
SHIFT alone is not sufficient to sustain hyperkalemia, as renal adaptation will excrete the excess extracellular K.
So decreased excretion is almost always necessary to cause and maintain significant hyperkalemia
It could be due to aldosterone deficiency- RAAS blockade (aldosterone inhibition) or receptor blockade (spironolactone and eplerenone)
So we have a patient, who has hyperkalemia, acidosis and renal failure
Intake is most likely reduced because of severe hyperglycemia, probably precipitated by urinary tract infection
Severe hyperglycemia causing shift of K along with water
Similarly, acidosis causing shifting out of K in exchange with H
ACEI inhibition can cause afferent vasodilatation and further decrease in GFR, especially in patient with reno-vascular disease (micro vascular or macro vascular) and advanced renal disease.
Prolonged application of torniquet, hemolysed sample can cause pseudohyperkalemia
Also in thrombocytosis (platlet counts&gt;6 lakhs) and severe leucocytosis (as in leukemias) the K can shift out of the cells after the sample is drawn and kept at room sample. If this is suspected, immidiate centrifugation after sample is drawn or storing the blood sample at 4 degrees is necessary
Because of the process of intrarenal urea recycling, the concept of TTKG has been discarded now. Halperin, KS Kamel 2011
Calcium is primarily given to protect the heart in presence of ECG changes, it helps to protect the heart from arrythmias transiently till further measures are taken to decrease the serum K
Saline if given in volume depleted, will increase the distal delivery of Na and water and promote K secretion
The diuretics increase the K excretion by similar mechanism, increasing the distal delivery of Na and water
Generalized skeletal muscle weakness, difficulty in weaning from a ventilator
Cardiac arrthymias
Paralytic ilies, especilly if occurs in postperative period, may cause bacterial transmigration, distention, anastomotic leaks, prolonged hospitalizaton
We have already gone the physiology of K in the previous topic. We will implement this in our case
What do you think is the major cause of hypokalemia here?