30 M HYPOKALEMIA PTB
3 0 year old male came to casualty with c/o involuntary movements of hands and tingling and numbness in upper limbs and abdomen since yesterday morning
Patient was apparently asymptomatic 20 days back then he developed fever insidious in onset, gradually progressive, low grade , intermittent not associated with chills and rigors and relieved by medication
He has a history of 4-5 episodes of vomitings 5 days back. Watery, non bilious ,non projectile, with food particles as contents.
Relieved by medication (unknown)
No c/o pain abdomen, loose stools
c/o burning micturition 2 days back, relieved now
H/o similar complaints in the past(7 years back) (hypokalemiac periodic paresis)
No h/o DM,HTN, asthma, epilepsy,cad, thyroid disorders
He used to take alcohol occasionally for the past 10 years and stopped taking 1 month back
He takes betel leaf(pan) once in 2 days for the past 10 years
O/E
Patient is conscious, coherent and cooperative well oriented to time ,place and person
No signs of pallor, icterus, cyanosis, clubbing, lymphadenopathy,edema
Vitals:
BP - 100/70mm hg
PR- 86 bpm
RR- 16 cpm
CVS EXAMINATION:
S1,S2 heard no murmurs
RS EXAMINATION:
trachea central
NVBS +
BAE +
P/A EXAMINATION:
Soft, non-tender
Bowel sounds heard
CNS EXAMINATION:
Hyporeflexia (due to hypokalemia) is seen
https://youtube.com/shorts/C_abIEr8Hs4?feature=share
DIAGNOSIS:
HYPOKALEMIA UNDER EVALUATION
INVESTIGATIONS:
Serum electrolytes
Na - 139 mEq/L
K - 2.3 mEq/L
Cl - 95 mEq/L
Ca - 1.01 mmol/L
Mg - 2.0
Urinary electrolytes
Na- 162
K - 7.3
Cl - 123
Urine Ph - 7.0
TREATMENT:
1)Inj. Kcl 50 mEq in 500 ml NS / IV over 5 hours
2) Inj. Zofer 4mg iv/OD
3)Inj. Pan 40 mg IV/OD
28/06/2023
AMC-30 YR M
S:
C/O PAIN ABDOMEN
O:
ON EXAMINATION:
PATIENT IS C/C/C
TEMP: 98 F
BP:100/70 mmHg
PR:86 BPM
RR: 16CPM
CVS:S1,S2 HEARD ,NO MURMURS
RS:BAE+,NVBS, NO ADDED SOUNDS
P/A: SOFT, NON TENDER
CNS:
TONE NORMAL IN ALL LIMBS
POWER 5/5 IN ALL LIMBS
A:
HYPOKALEMIA UNDER EVALUATION
P:
1.INJ OPTINEURON 1 AMP IN 100 ML NS IV/OD
2.TAB.PCM 650 MG PO/SOS
3.INJ. KCL 2 AMP IN 500 ML NS IV OVER 5 HOURS
4.SYP. POTCHLOR 15 ML PO/TID
29/06/2023
AMC-30 Y/M
S:
C/O GENERALISED WEAKNESS
O:
ON EXAMINATION:
PATIENT IS C/C/C
TEMP: 98 F
BP:110/70 mmHg
PR:88 BPM
RR: 17CPM
CVS:S1,S2 HEARD ,NO MURMURS
RS:BAE+,NVBS, NO ADDED SOUNDS
P/A: SOFT, NON TENDER
CNS:
TONE NORMAL IN ALL LIMBS
POWER 5/5 IN ALL LIMBS
A:
PULMONARY KOCHS WITH HYPOKALEMIA
P:
1.INJ OPTINEURON 1 AMP IN 100 ML NS IV/OD
2.INJ. KCL 2 AMP(40MEq) IN 500 ML NS IV OVER 5 HOURS
3.SYP. POTCHLOR 15 ML PO/TID
Started ATT
4. TAB.ISONIAZID -390mg po/od
5.TAB. RIFAMPICIN- 780mg po/od
6.TAB.PYRIZINAMIDE -1950mg po/od
7.TAB. ETHAMBUTOL 1625mg po/od
8.TAB. PYRIDOXINE 40MG PO/OD
29/06/2023
AMC-30 YR M
ATT STARTED ON 29/06/2023
S:
C/O GENERALISED WEAKNESS
O:
ON EXAMINATION:
PATIENT IS C/C/C
TEMP: 98 F
BP:110/70 mmHg
PR:88 BPM
RR: 17CPM
CVS:S1,S2 HEARD ,NO MURMURS
RS:BAE+,NVBS, NO ADDED SOUNDS
P/A: SOFT, NON TENDER
CNS:
TONE NORMAL IN ALL LIMBS
POWER 5/5 IN ALL LIMBS
A:
PULMONARY KOCHS WITH HYPOKALEMIA
P:
1.INJ OPTINEURON 1 AMP IN 100 ML NS IV/OD
2.INJ. KCL 2 AMP(50MEq) IN 500 ML NS IV OVER 5 HOURS
3.SYP. POTCHLOR 15 ML PO/TID
ATT STARTED
4. TAB.ISONIAZID -390mg po/od
5.TAB. RIFAMPICIN- 780mg po/od
6.TAB.PYRIZINAMIDE -1950mg po/od
7.TAB. ETHAMBUTOL 1625mg po/od
8.TAB. PYRIDOXINE 40MG PO/OD
PAJR GROUP DISCUSSION
[10/26, 11:06 AM] KIMS UG 2021: According to his history... He had same complaint before he had tb sir
[10/26, 11:07 AM] KIMS UG 2021: I think it's because of his low k+ but not related to side effects of tb drugs
[10/26, 1:04 PM] Rakesh Biswas: How does low potassium periodically become low enough to cause paralysis in certain people?
[10/26, 1:18 PM] KIMS UG 2021: Sir he already had past history of paresis...
[10/26, 1:40 PM] Rakesh Biswas: Exactly why do some people have periodic hypokalemic paralysis? Which gene and protein product are involved?
[10/26, 2:25 PM] KIMS UG 2021: Calcium or sodium channel mutations sir....
[10/26, 2:26 PM] KIMS UG 2021: Genes
[10/26, 2:28 PM] KIMS UG 2021: It can be hereditary or sporadic,
If sporadic then mutation of calcium or sodium channel encoding genes sir
[10/26, 4:04 PM] Rakesh Biswas: And how does the mutation lead to muscle paralysis and tetany?
[10/27, 7:21 AM] ~Tejaswi Alluri KIMS UG 2021: Normal muscle contraction:
Depolarization - efflux of ca+ and Na+
Normal muscle relaxation:
Hyperpolarization - influx of k+
But in condition of mutations,
Depolarization state is prolonged (due to prolonge opening ca+2and Na+ channels) and due to Hypoakalemia muscle relaxation cannot occur.
[10/27, 7:24 AM] KIMS UG 2021: Sir, I think this could be one of the reason according to my 1st year knowledge
[10/27, 7:46 AM] Rakesh Biswas: Can you cite a few references with quotes that also supports this view?
[10/27, 8:02 AM] KIMS UG 2021: Ok sir... Sir this can also be taken from ou pharmacology chapter epilepsy??
[10/27, 8:06 AM] Rakesh Biswas: Read scientific journal articles through internet search engines
Text books that don't have any scientific references are largely unscientific.
Search for hypokalemic periodic paralysis mechanisms
[10/27, 8:06 AM] KIMS UG 2021: Ok sir, I understood
[10/27, 8:10 AM] KIMS UG 2021: Sir this article is exactly matching the patient's condition
[10/27, 8:19 AM] Rakesh Biswas: Please quote from the article as to how.
Don't share screenshots as they can't be archived
[10/27, 8:21 AM] Rakesh Biswas: This is kind of a conceptual scientific reference for what you paraphrased earlier from your text book reading?
[10/27, 8:25 AM] KIMS UG 2021: Yes...
The similar thing I found in this article
[10/27, 8:30 AM] Rakesh Biswas: How's the article content exactly matching your patient's condition? How can we be even sure that your patient actually has hypokalemic periodic paralysis as well as those mutations?
Did you see the two CNS patients we demonstrated yesterday in the opd?
[10/27, 8:36 AM] KIMS UG 2021: Sir usually if a person is having mutations or hereditary history of these ion channelopathy.... there can be the same kind of past history of paralysis
[10/27, 8:47 AM] Rakesh Biswas: Share his history in detail. Check out detailed histories available in similar patients globally through search engines as well as locally logged by our past students through our departmental dash board here 👇
http://medicinedepartment.blogspot.com/2022/02/?m=1
[10/28, 7:56 PM] : this patient weight was 67 when we started him on ATT (5 tablets / day)
later when they started him on continuation phase his weight is 59 kgs ( so gave him 4 tablets / day sir )
[10/28, 9:15 PM] Rakesh Biswas: How did you know this?
This patient's TB was an incidentaloma!!
30/M came with complaints of involuntary movements associated with tingling and numbness of bilateral upper limbs and abdomen since 1 day.He had 1 episode of low grade fever which was relieved on taking medication 20 days ago. He has history of hypokalemic periodic paralysis 7 years ago. He did not experience any weight loss , night sweats, fever , cough , dyspnea , anorexia and did not produce sputum.
Clinical examination showed hyporeflexia apart from it everything is normal. Laboratory tests showed serum potassium of 2.3 mEq / L.On a routine screening chest X ray showed left upper lobe consolidatory changes.Sputum samples showed ACID FAST BACILLI.Patient was started on ATT.
One out of four individuals are being effected with tuberculosis in india.
Asymptomatic individuals are also highly suspected to have tuberculosis in India.
[10/28, 8:13 PM] : sir, do I need to mention that we have not done mantoux test in this case ?
Here in this case a routine screening with chest x ray made us supect tuberculosis. If it was not done he might be left undiagnosed and also left untreated.
Can I mention this case as subclinical tuberculosis sir?
even though his appetite is normal there is significant weight loss ? Does it mean he is not recovering well?
I always have this question in mind , Seeing these many confirmed cases of tuberculosis, I always wonder how many of their family members are effected with the same and go undiagnosed and untreated.
taking this case as an example what if his family is also asymptomatic ? They might be spreding to many others in their neighbourhood. How can we reduce the number of cases being undiagnosed and untreated.
[10/28, 9:16 PM] Rakesh Biswas: This is the principle of tuberculosis contact tracing
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