2. Fluid and electrolyte disturbances
• Most common clinical problems encountered in the
intensive care unit (ICU).
• Increased morbidity and mortality among critically ill
patients.
• 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
• Critical disorders like trauma, sepsis, brain damage, and
heart failure cause disturbances in fluid and electrolyte
homeostasis.
• Mechanisms: reduced perfusion to the kidney
(hypovolemia or hypotension), activation of hormonal
systems such as RAAS and AVP, Renal tubular damage.
• Most important: inappropriate administration of fluid and
electrolytes
4. Fluid and electrolyte disturbances
• Formulae to guide the therapy:
– All formulae regard the patient as a closed system
– none takes into account ongoing fluid losses that are
highly variable between patients
– Therapy must be closely monitored with serial serum
and urine electrolyte measurements.
Semin Dial. 2006 Nov-Dec;19(6):496-501.
5. Dysnatremias
• Prevalence 20-30% in some studies
• hypo- and hypernatremia in ICU, independent
risk factors for poor prognosis
• Disorders of water balance
• Often iatrogenic
Can J Anaesth 2010 Jul;57(7):650-8
7. Hyponatremia
• Commonest electrolyte disorder in
hospitalized patients
• Mostly iatrogenic- wrong fluids, surgical
wards and postoperative patients
• concept of “maintenance fluids”
8. Overview
• Definition
• Physiology of Na and H2O
• Case
• Classify
• How urgent is the treatment and whom to treat?
• Treatment guideline.
9. Hyponatremia- Define it
• Relative water excess
Sr Na < 136 Meq/ L
– Low water and lower sodium content in the body
Hypovolemic hyponatremia
Extracellular fluid volume contraction (true volume depletion)
Syndrome of appropriate ADH secretion
11. Hyponatremia- Define it
– Normal or excess Na, and still higher H2O content
CHF, Nephrotic syndrome, cirrhosis of Liver
Non osmotic release of ADH
“Effective” circulating volume contraction
13. Don’t forget ADH…..
• Water surplus/ excess alone….
– Excess free water (electrolyte free water) ingestion alone –
will result in large quantity of maximally diluted urine
– So only water surplus – cannot cause/ sustain hyponatremia
– ADH – almost always present
– What we want to know is why is the ADH present?
14. Symptoms and signs
of hyponatremia
• None
• Headache
• Lethargy
• Dizziness and ataxia
• Mild confusion
• Psychosis
• Seizures
• Coma
27. Endocrine factors-Hypothyroidism
• Hypothyroidism
– commonest electrolyte derangement in hypothyroid
– Hyponatremia : 45% of hypothyroid patients
– Increased serum creatinine
– Decreased glomerular filtration
– Decreased sodium reabsorption
⇓renal ability to dilute urine- water excretion
So a very much
Correctable factor
that can lead to
hyponatremia
28. Endocrine factors- Addisions disease
• Pigmentation
• salt craving
• hypotension
• hyperkalemia
• hypersecretion of ADH:
– reductions in BP and cardiac
output
– salt wasting with resultant
volume depletion
– Hypovolemia stimulates the
release of ADH
– Hyponatremia corrected by
cortisol and volume repletion,
shuts off ADH release.
29. 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
since 5 days. c/o decreased urine output.
• Confused since 1 day- GTCs 1 hr ago
• Hospitalized: 60 kg (previously recorded)
– HR- 100, BP 130/70, low JVP, post ictal state.
– Appeared volume depleted
30. Case 1
• Treatment:
– Catheterized- 200 ml immediately removed,
blood tests sent, IV access, Ryles tube
– FPBS- 106, IV NS 1000 ml over 1/2 hr
– Noted urobag to be full- staff assumed retention,
everyone happy.
31. We got the blood tests…..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
32. 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
33. Case 1
• Why did this happen?
• Risks?
• What went wrong?
• What do we do next?
34. Case 1- why did this happen
• Lets calculate what went in and how much should have the
Sr Na changed.
– TBW= 30 L (50% of weight in females)
– Given 150 Meq/ L of 0.9 % NS (ie 1 L of H2O + 150 Na)
– Na deficit (Na to be replaced to achieve a particular Sr Na
Level) = TBW (desired Na- actual Na)
– 150 Meq/L = 31 L (x- 125 Meq/L).
– “X” is what the Na should be, if we replace 1 L of 0.9% NS
– X = 5 Meq/ L
35. Why did this happen ?
• ADH shut off- volume
replacement
• Free water diuresis-
– Electrolyte free water is
excreted
– So if H2O is removed from
body, Na concentration
rapidly increases
36. Risks
• Osmotic demyelination
syndrome (ODS or CPM)
– Under estimated incidence
– Critically ill ICU patients,
difficult to diagnose
pons
Non pontine areas
37. Pathogenesis and clinical features
• Chronic hyponatremia-
brain cell adaptation
– Lose osmolytes & H2O
– Protection against cerebral
edema
• Rapid correction- no time
for adaptation
– Brain cells shrink- apoptosis
• Symptoms
MRI changes are
Late.
Mimics any other diffuse
Encephalopathy.
Brain
edema
adaptation
38. What went wrong?
• Classify hyponatremia
– Acute Vs Chronic is the only useful one for treatment
– Most chronics have an acute component
– In our case, even before we classified it, we corrected it
inadvertently
– Lady definitely had and acute component, excessive water
drinking….
• Why did the Na correct so rapidly even with 150 Meq/L
of Na?
39. 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 ⇑ by 5 Meq/ L
• Why did it go up so rapidly?
The concept of tonicity balance
What goes in and what comes out?
40. 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
41. 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
42. Why GTCs at Na of 125??
• 1st
- we check Venous Na, not arterial.
– Brain sees arterial Na, not venous.
– Arterial Na 3-5 Meq/L lower than venous Na
• 2nd
and more important-
– Post GTCs: seizures increase Sr Na!!!
– During seizures, muscle cells produce osmotically
effective molecules
– So water shifts in muscle cell- Sr Na can rise by 10 to 15
Meq/L after seizures
43. Don’t forget the water in GI tract..
• Most cases of acute on chronic hyponatremia,
occurring at home- solute free water intake/
fruit juices etc – water source
• Insert RT in hyponatremic convulsion-
remove water in stomach if its there
44. Remember about K correction….
• Most body K – intracellular
• K replaced for correction of hypokalemia:
– Enters the cells, intracellular Na comes out
– So giving 80 Meq/L of K is equivalent to giving
Na
– K replacement is equivalent to giving Na
45. Back to our Case
• Lower the Na: 1 L of 5D = will decrease Na by 5Meq/L
– 3910/30= 130
• Stop further diuresis of free water: DDAVD
(desmopressin)
– Ideally IV 2 to 10ug, till urine output < 100 ml/hr
– Used 20 ug intranasal- decreased diuresis
• 6 hrly monitoring of Sr and urine electrolytes
• Replace what comes out (urine)- volume + electrolytes
46. Replace what comes out (urine)
• Urine 100 ml/ hr, Urinary Na + K = 70
– Give half NS with Na content of 75 meq
– This will prevent further rise
• Urine Na + K 40 Meq/ L
– 500 ml 5D + 500 ml 0.45 NS = 37 Meq/ L of Na
• Free water restriction to < 1 L/ day
• Oral K replacement, isotonic fluid of KCL if IV
47. Case 2
• 37/F, No significant past history
• DUB- advised hysterectomy.
• Low risk, pre-op investigations- WNL
• Cardiac evaluation – normal
• Surgery under SA, lowest intra-op BP- 100/60
48. Case 2
• Received 1L RL (Na- 130 +4 K) intra-op, post-
op: 1000 ml of 5% D and 500ml of NS over
3hs.
• GTCs
– CBC, Sr Ca, Sr Mg all normal
– Na- 125
Why did the lady develop hyponatremia acutely?
49. Case 2
• Urine output- 1.5 L once she was catheterised,
till she convulsed.
• Urinary Na- 190, K- 60
50. Tonicity balance
50 kg lady
Input
2.5 L
i.e. 2.5 L of H2O
+ 210 Meq (Mmols)
Of Na
Body compartment
Na and water Content
Output
1.5 L urine
U Na + K = 250
i.e. 1.5 L of water
And 375 mol Na +K
25 L TBW in 50kg female
25 L of water
3500 Mmols Na
51. Tonicity balance- new body content
of Na and water
Body compartment
New Na and water Content
25 L TBW in 50kg female
Water= 25+2.5-1.5=
26 L
Na: 3500+ 210-
375
=3335
Sr Na =3335 /26
127
And that was
Our Sr Na
52. Why hyponatremia?
• Obviously ADH was on board……..
• Where did it come from.??
• Pain & nausea are very powerful stimulants…
53. Why convulsions at 125?
• Young female, small muscle size
• Acute hyponatremia..
• Treatment
– 3% 200 ml to acutely raise the Sr Na by say 5
Meq/L
– Then correct the remaining over next 24 hours
– Relief of nausea and pain will help correct ⇓ Na
54. Summary of guidelines for therapy
• Classify acute Vs Chronic- history, change in
medications
• Assess volume status
– Most reliable hematocrit and total Sr. proteins
– Urine electrolytes (UNa < 10)
– Hemodynamic and clinical: least reliable
• Therapeutic considerations in acute hyponatremia and
diagnostic considerations in chronic hyponatremia
55. Summary of guidelines for therapy
• Acute component of Chronic:
– Raise Na by < 5 Meq/L, use 3% NS
– Later fluid restriction and find the cause
• Ask 2 questions in the patient with low Na
– Why is the ADH present?
– Will the release of ADH cease and cause rapid
water diuresis?
57. • Symptoms
• of hyponatremia may not be apparent in
ventilated and
• sedated patients in the ICU, and worsening
of cerebral
• edema may lead to catastrophic
consequences such as
• brainstem herniation and respiratory arrest.
60. 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
61. 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
62. 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
63. An increase in plasma potassium
concentration and/or potassium intake
64. An increase in aldosterone secretion
Hyperkalemia
Renin angiotensin
Aldosterone system
(RAAS)
Na channel
Aldosterone deficiency,
blockade
65. 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
66. 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
69. Hyperkalemia
• Increased intake: K adaptation, rapid
• Shift: intracellular to extracellular, alone again not
enough to sustain hyper K.
• Decrease excretion: almost always present
– Aldosterone
– Decreased distal delivery of Na/ water
– Renal dysfunction
70. 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
71. Case1: examination
• ECG: HR of 30, broad QRS, CHB like pattern
• Rest vitals stable
• Higher functions normal
• Quadriparesis (grade 2 power, absent reflexes)
72. 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
75. Case analysis
• Decreased renal excretion (almost always)
• Was started on ramipril (ACEI) for HT
– 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
77. Case analysis
• The patient was also
started on
spironolactone which
blocked aldosterone
action
• NSAIDS for fever
– Deceased GFR
– Renal failure
78. 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
– High capacity K channels (big K or Maxi K)
– Activated of high flow (water and Na delivery)
– Activated by K depletion
– Aldosterone independent action
79. Another K channel: intercalated cells
• H-K exchanger in IC
cells of CCD
• Activated in K depletion
• Absorbs K+ and
secretion of H+
80. Evaluation of hyperkalemia
• Exclude Pseudohyperkalemia
– potassium movement out of the cells during or after
the blood collection
– Torniquet
– Thrombocytosis, high WBC counts (leukemias)
81. 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
– < 15 mmol/gm in K depletion
– >200 mmol/gm in hyperkalemia
–
82. 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
83. Case 1
• NSAIDS: worsening of RFT (GFR)
• PG synthesis inhibited
– PG inhibit renin –reduce aldosterone
• So in this patients, almost all things to increase
his K has been done
– ACEI, aldosterone blockade
– NSAIDS
84. Treatment of severe hyperkalemia
• Calcium: if hypocalcemia or ECG changes
• Shift inside the cells:
– Insulin alone (hyperglycemia) or with 25 %
– Dextrose
– B2 agonist
– Bicarbonate if acidosis
85. Treatment
• Excretion
– Saline, especially if depleted
– Thiazide and loop diuretic
– 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
86. 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
87. The message..
• Increase intake- not sufficient
• Hyperkalemia is always a kidney problem
• Consider shift
• Drug history very important
• Assess excretion
– Urine electrolytes- distal Na delivery
– Aldosterone deficiency/ block
– Urine K/ Creatinine is important
90. In ICUs….
• Upto 20% of patients
• Symptoms: mainly neuromuscular
• Risks:
– Respiratory muscle weakness, difficult to wean
– Life threatening cardiac arrthymias
– Paralytic ileus, risk of transmigration, nutrition
91. hypokalemia
• Low intake: possible, if prolonged, critically ill
– Kidneys can decrease excretion < 20 Meq/ day
– Low intake alone, not be sufficient unless severe
• Shift very important in this settings, drugs
• Excretion: diuretics
– Drugs like amphoterecin B
– Non absorbable anions- penicillins
92. 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
94. 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
95. 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?
96. Case analysis
• Intake- poor, nausea
– Likely lower body content: thiazides
– Hyperglycemia (sepsis)- osmotic diuresis
• Initial K normal: shift out of cells
– Hyperglycemia
– Insulin deficiency
100. Case analysis: Renal excretion
• Distal delivery of Na and K: NS infusion
• Diuretics: increase distal delivery of Na and
Water
• Hyperglycemia: Osmotic diuresis
104. Renal excretion: non-reabsorbable anions
• Like β-hydroxybutyrate in DKA,
– 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
106. Extra renal loses
• Loss of gastric secretions (vomiting, aspiration)
– Little K in gastric juice
– Loss of H+ met alkalosis increased HCO3 + Na
– Na exchanged with K
• Diarrhea: K content in intestinal juices (30- 50 meq)
•
107. Case analysis
• Decreased intake- yes, low stores (thiazides)
• Shift: definitely
– Insulin
– Beta stimulation
• Excretion: NO. Urine Na and K,
appropriately low
Editor's Notes
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 – 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.
Hypo or hypernatremia present at admission or developing in the ICU are independent risk factors for poor outcome.
Hyponatremia is relative water excess, while hyernatremia is relative water deficiency.
This is not a single topic. Actually it’s 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 “No hyponatremia is enough hyponatremia”. 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 terms…. 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
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 – 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 it’s a diagnosis of exclusion.
No treatment available and so only thing we can do is prevention.
The main problem is shrinking of the brain cells, if the hyponatremia is chronic (more than 48 hrs duration)- the brain cells in chronic hyponatremia lose osmolytes (sodium, potassium, chloride, and organic osmolytes such as myoinositol, glutamate, and glutamine) and water from brain cells, which provides protection against cerebral edema.
Symptoms include- coma, seizures, locked in state, flaccid quadriparesis.
MRI changes appear approximately 3 weeks after the insult, so we need to rule out other causes of diffuse encephalopathy. So initially it’s a diagnosis of exclusion. MRI changes appear approximately 3 weeks after the insult, so we need to rule out other causes of diffuse encephalopathy. So initially it’s a diagnosis of exclusion.
It’s a disorder with high mortality and morbidity, no specific treatment is available, so the only thing that can be done 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.
Now there can be many causes of GTCs in post-operative patient- cortial venous thrombosis, metabolic, drugs used and many more…. But this being a session on hyponatremia, obviously this is going to be the reason.
So again we will discuss the tonicity balance
Good urine output for a post operative patient with say 4 hours
Remember Sr concentration of Na = total body content of Na / total body water.
Where did this 3500 mmol (meq)/ L of Na come from?- 25 L multiplied by Sr Na conc (140)
Use 3% NS to raise the Na by &lt; 5 Meq/ L
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;
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?