In principle, ADN can lead to clinical symptoms in all autonomously innervated organs (Strian 2013).
The typical complaints of patients with cardiovascular ADN are:
This results from vagus damage and the resulting sympathicotonic overload. After an average 5-year latency period, damage to sympathetic nerve fibers occurs, resulting in (partial) regression of tachycardia. Overall, however, the heart rate remains higher than in healthy individuals (Schönauer 2007).
- asympathicotonic orthostatic hypotension due to damage to the sympathetic nervous system with a lack of reflex tachycardia during standing exercise and a drop in both systolic and diastolic blood pressure (Herold 2020)
- exercise intolerance (Häring 2011)
- Painless myocardial infarction (lack of pain perception due to damage to sensory nerve fibers [Schönauer 2007])
- painless myocardial ischemia
- Heart rate variability decreased up to frequency rigidity during
- resting ECG
- 24 h ECG
- maximal inspiration and expiration (normally the difference of the heart rate is < 9 / min)
- Orthostasis test
- Valsalva compression test (Herold 2020)
- QTc prolongation (German Medical Association 2016)
- abolished or reversed circadian blood pressure curve with increased blood pressure values at night (so-called non- dipper)
- perioperative instability (Häring 2011)
-
2. ADN of the gastrointestinal tract (parasympathetic damage rarely occurs in this area):
- gastroparesis with pressure in the upper abdomen and feeling of fullness
- postprandial hypoglycemia (occurs about 30 min p.p. [Hien 2010])
- Esophageal motility disorder
- Disturbance of gallbladder contractility with increased formation of gallstones (German Medical Association 2016)
- anorectal dysfunction with incontinence
- postprandial diarrhea with alternating phases of constipation due to motility disorders in the lower intestinal segments (Siegenthaler 2006; Herold 2020)
Diabetes type 1 patients should also always be examined for celiac disease if they have typical symptoms, as this occurs more frequently than average in them (Kasper 2015).
-
3. ADN of the urogenital system (parasympathetic damage often occurs in the urogenital system):
- Early symptoms are:
- the bladder can no longer be emptied completely
- a full bladder can no longer be perceived (Kasper 2015)
- erectile dysfunction with failure to achieve a spontaneous erection at night or in the morning
- Bladder emptying disorders in bladder atony with residual urine formation and resulting predisposition to recurrent urinary tract infections (Herold 2020)
- Incontinence and decrease in bladder capacity due to delayed bladder contractility (Kasper 2015)
-
4. ADN of the neuroendocrine system:
- Decreased perception of hypoglycemia due to reduction or absence of hormonal counter-response in the presence of hypoglycemia (Kasper 2015)
- Reduced release of catecholamines under physical and orthostatic stress (Herold 2020)
- 5. ADN of thermoregulation: ADN of thermoregulation leads to:
- Vasodilation
- Decreased sweat secretion
The dry and warm diabetic foot typical of diabetics [Herold 2020]) exist due to decreased sweat secretion and vasodilation.
Due to the disturbance of the sympathetic nervous system, there may also be hyperhidrosis of the upper extremities (Kasper 2015).
In this case, there are disturbed pupillary reflexes and reduced brightness adaptation (Häring 2011). Spontaneous fluctuations of the pupil diameter are - compared to healthy people - only diminished.
If sympathetic damage is in the foreground, there is miosis (Bundesärztekammer 2016).
- 7. ADN of the respiratory tract:
Respiratory drive is decreased in hypoxemia and hypercapnia. Apnea and respiratory arrest may also occur (Häring 2011).
The skin is - due to lack of impulses to connective tissue and skin - doughy and atrophic. This is particularly observable in the "diabetic foot" (Hien 2010).