Diabetes HTN And Right Foot Injury

K.Shubankar 184


A 65 Year old male with Diabetes, Hypertension and Right foot injury.


This is an online E-Log book to discuss our patient's de-identified data shared after taking his/her/Guardian's signed informed consent. Here, we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve these patient's clinical problems with collective current best evidence-based inputs. This E-log also reflects my patient-centered online learning portfolio and your valuable inputs in the comment box are welcome.



I've been given this case to solve in an attempt to understand the topic of "Patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history, Clinical findings, investigations and come up with a diagnosis and treatment plan.



CONSENT AND DEIDENTIFICATION:


The patient and the attenders have been adequately informed about this documentation and privacy of the patient is being entirely conserved. No identifiers shall be revealed through out the piece of work whatsoever.




This case is about a 65 year old Gentleman who was an RTC driver 15 years back , came with 


Chief Complaints:


Decreased urine output (dysuria, hematuria, burning micturition ) since 20 days


SOB since 10 days 


HOPI:


The patient was apparently asymptomatic 10 years ago then he felt weak and not well for a few days for which he visited local hospital and was diagnosed to be Hypertensive 

He was kept to Antihypertensives and now is on

Atenolol Amlodipine 50mg/5mg



5 years ago:


The patient one day was helping someone who was cutting a tree by holding the branch which was being cut with the help of a rope

He got injured by a stone in the rope to his left palm

This was followed by pain, swelling and blackish discolouration 

Then was when he was diagonosed incidentally as diabetic and was kept on medication 

He is now on Tab. Metformin 500mg




4 years ago:


He drank and drove following which he had an accident and was taken to hospital from there.

He had  

Fracture to his Left ribs (5,6,7) at mid clavicular line And Punctured his lung 


30 days back:


While he was going out for work, he stepped over a sharp stone which penetrated through his right little toe

He used medications from the local medical store for about 10 days 


He noticed:


1. Increase in pain gradual


2. Edema till his knee which was gradual


3. Bleb formation of about 3*3 cm on the dorsum of his foot which he ruptured by piercing a safety pin through it

There was bleeding from the site after piercing and it continued for a few days and formed into an ulcer.


4. Low grade on and off fever 


5. There was also difficulty in urination 

Burning micturition 

Hematuria

Reduced urine output


He then went to a government hospital in Nalgonda and was diagnosed to be AKI on CKD and was transferred for private hospital  for dialysis


There he developed SOB of grade 2-3, orthopnea and PND 


He undergone through first session of Dialysis 



He had itching at his abdomen, back and left and right Axilla 


Then he was shifted to another hospital for Dialysis due to money restraints.


Timeline of events:






Past History:


Hypertensive since 10 years

Diabetic since 5 years

No History of Asthma, tuberculosis, epilepsy. 


Family History:


The patients mother was a diabetic

None of the other family members have similar complaints


Drug History:


Atenolol+Amlodipine 50mg/5mg

Metformin500mg

No known allergies


Personal history:


Diet- mixed

Appetite-reduced since 3 days

Sleep - inadequate

Bladder - decreased  

Bowel- regular 

Alcoholic 90ml everyday since 40 years

Chronic smoker 1 pack since 40 years



General Examination:


The patient is conscious coherent cooperative, and well oriented to time place and person

He is moderately built and nourished


Pallor- absent

Icterus- absent 

Cyanosis- absent

Clubbing-absent

Edema- present pitting Type 

Lymphedenopathy - absent


VITALS:


Temperature- afebrile

Pulse rate- 68 beats per minute

Respiratory rate- 22 breaths per minute

B.P- 160/90 mm hg

SpO2- 99% at room air







SYSTEMIC EXAMINATION:


*CVS: 

             S1and S2 are heard 

            No murmurs are heard


*Respiratory system:


                     BAE- positive

                  Dyspnoea- present

                 Breath sounds- decreased breath sounds in right side

                 Vesicular breath sounds are normal

                  Rt side Fine Crepts present 

                 


*Central nervous system:

                 Patient was conscious coherent and cooperative.

                 Speech was normal.

                No meningeal irritation signs 

               GAIT - Normal


*Abdomen:

                Soft and non tender


















INVESTIGATIONS:











Provisional Diagnosis:


AKI ON CKD SECONDARY TO RIGHT LOWER LIMB CELLULITIS(DIABETIC FOOT)

Treatment:



31/12/2021
IVF.NS OR RL UO+50ml/ hr
INJ Lasix 40mg iv/BD
INJ Piptaz 2.25gm iv / TID
INJ nodosis 500mg po/TID
CAP BioD3 0.2mg po/Od
Mgso4 dressing for R. Lower limb cellulitis
RLL elevation 
Monitor vitals
Charting
GRBS 6th hrly
Inj HAI s/c 8am 2pm 8 am

01/01/2022
Add on
Tab nicardia 5mg Po/Bd

02/01/2022
Add on
Slat restriction
Fluid restriction 
Tab nicardia 10mg

03/01/2022
Add on 
Pan 40mg/bd

06/01/2022
Add on
Inj clindamycin 600mg Iv/TDS

08/01/2022
Add on

Oint Thrombophob




Questions Discussed:

1)Adipocytes and Hypertension effect on Blood Vessels?


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371623/



In a healthy person adipose tissue maintains a specifically balanced adipokine profile, which modulates vascular homeostasis via endocrine and paracrine pathways . 


*Excessive accumulation of adipose tissue may alter the expression of the adipokine profile and consequently the physiological effects of adipokines on the vessels. Excessive weight gain contributes to increased blood pressure in most patients with essential hypertension. Blood pressure is a function of cardiac output and peripheral resistance.


* Weight gain leads to increased cardiac output and blood volume, which might be related to activation of SNS and RAS, and to physical compression of the kidneys by fat accumulation within and around the kidneys and excessive visceral fat. SNS activation and physical compression of the kidneys both cause activation of the RAS, and pharmacological blockade of either the RAS or the SNS attenuates obesity induced hypertension by at least 50-60%. 


*Several mediators in the obesity-associated hypertension have been suggested, including hyperinsulinemia, angiotensin II, FFAs and leptin. Hyperinsulinemia could lead to a rise in blood pressure by enhancing sodium retention. Adipocytes secrete angiotensinogen, which can be converted to angiotensin I and then angiotensin II, a potent vasoconstrictor and promoter of sodium and water absorption.

 
*FFAs could promote hypertension by means of adrenergic stimulation, increase in oxidative stress, endothelial dysfunction, or stimulation of vascular cell growth. Leptin activates SNS by stimulating opiomelanocortin neurons, with subsequent activation of central nervous system melanocortin 4 receptors. The physiological importance of leptin in blood pressure regulation has been demonstrated in animal models. Obese Ob/ob mice deficient in leptin have significantly decreased blood pressure. Increased peripheral resistance due primarily to changes in vascular structure and function appear to be the fundamental abnormality in hypertension. 


*Adipokines induce the functional and structural changes in the vessels by endothelial dysfunction, VSMC proliferation and migration and vascular inflammation, thereby regulating vascular responses to constrictor and dilator stimuli and contribute to the increased arterial pressure.

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